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8. Characterization of the novel HLA-DPA1*01:03:19 allele by sequencing-based typing

Author

Cargou, M., Andreani, M., Locatelli, Franco, Blouin, L., Visentin, J., Locatelli F. (ORCID:0000-0002-7976-3654), Cargou, M., Andreani, M., Locatelli, Franco, Blouin, L., Visentin, J., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

HLA-DPA1*01:03:19 differs from DPA1*01:03:01:02 by one nucleotide substitution in codon 190 in exon 4.

Published
2020

9. Les auteurs

Author

Adotévi., O., Amé-Thomas., P., Arnulf., B., Baron., C., Batteux., F., Beauvillain., C., Bérard., F., Blancho., G., Bourdenet., G., Boyer., O., Caillat-Zucman., S., Candon., S., Carapito., R., Carcelain., G., Carnoy., C., Cesbron., J.-Y., Chevailler., A., Chollet-Martin., S., Colombo., B., Contin-Bordes., C., Coutant., F., Dantal., J., de Carvalho Bittencourt., M., de Chaisemartin., L., Delfau-Larue., M.-H., Desplat-Jégo., S., Dragon-Durey., M.-A., Dubucquoi., S., Dumestre-Perard., C., Fischer., A., Fisson., S., Flament., H., Fournel., S., Galaine., J., Garraud., O., Godet., Y., Gorochov., G., Gros., F., Gubler., B., Guffroy., A., Hacein-Bey-Abina., S., Hoarau., C., Hüe., S., Kaplanski., G., Kervella., D., Kolopp Sarda., M.-N., Labalette., M., Lambotte., O., Le Gouvello., S., Le Naour., R., Lelièvre., J.-D., Lemoine., F., Liégeois., S., Martinet., J., Miyara., M., Moins-Teisserenc., H., Molinier-Frenkel., V., Nel., I., Pagès., F., Paul., S., Picard., C., Radosavljevic., M., Renaudineau., Y., Rosain., J., Rosenzwajg., M., Seillès., E., Soulas-Sprauel., P., Sterlin., D., Tartour., É., Taupin., J.-L., Thibault., G., Tiberghien., P., Toubert., A., Visentin., J., Vitte., J., Vivier., É., Watier., H., and Weiss., L.

Published
2023
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10. Characterization of the novel HLA-DPA1*02:15 allele by sequencing-based typing

Author

Blouin, L., Andreani, M., Locatelli, Franco, Guidicelli, G., Visentin, J., Locatelli F. (ORCID:0000-0002-7976-3654), Blouin, L., Andreani, M., Locatelli, Franco, Guidicelli, G., Visentin, J., and Locatelli F. (ORCID:0000-0002-7976-3654)

Abstract

HLA-DPA1*02:15 differs from HLA-DPA1*02:06 by one nucleotide substitution in codon 218 in exon 4.

Published
2019

18. Donor Specific Anti-HLA Antibodies Towards HLA Cw and HLA DP Should Be Considered as Pathogenic in Kidney Transplantation.

Author

Merville, P., primary, Martinez, C., additional, Del Bello, A., additional, Kejji, S., additional, Couzi, L., additional, Guidicelli, G., additional, Lepreux, S., additional, Visentin, J., additional, Congy-Jolivet, N., additional, Rostaing, L., additional, Taupin, J., additional, Kamar, N., additional, and Bachelet, T., additional

Published
2014
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19. TRANSPLANTATION CLINICAL 1

Author

Schachtner, T., primary, Reinke, P., additional, Dorje, C., additional, Mjoen, G., additional, Midtvedt, K., additional, Strom, E. H., additional, Oyen, O., additional, Jenssen, T., additional, Reisaeter, A. V., additional, Smedbraaten, Y. V., additional, Sagedal, S., additional, Fagerland, M. W., additional, Hartmann, A., additional, Thiel, S., additional, Zulkarnaev, A., additional, Vatazin, A., additional, Vincenti, F., additional, Harel, E., additional, Kantor, A., additional, Thurison, T., additional, Hoyer-Hansen, G., additional, Craik, C., additional, Kute, V. B., additional, Shah, P. S., additional, Vanikar, A. V., additional, Modi, P. R., additional, Shah, P. R., additional, Gumber, M. R., additional, Patel, H. V., additional, Engineer, D. P., additional, Shah, V. R., additional, Rizvi, J., additional, Trivedi, H. L., additional, Malheiro, J., additional, Dias, L., additional, Martins, L. S., additional, Fonseca, I., additional, Pedroso, S., additional, Almeida, M., additional, Castro-Henriques, A., additional, Cabrita, A., additional, Costa, C., additional, Ritta, M., additional, Sinesi, F., additional, Sidoti, F., additional, Mantovani, S., additional, Di Nauta, A., additional, Messina, M., additional, Cavallo, R., additional, Verflova, A., additional, Svobodova, E., additional, Slatinska, J., additional, Slavcev, A., additional, Pokorna, E., additional, Viklicky, O., additional, Yagan, J., additional, Chandraker, A., additional, Diena, D., additional, Tognarelli, G., additional, Ranghino, A., additional, Bussolino, S., additional, Fop, F., additional, Segoloni, G. P., additional, Biancone, L., additional, Leone, F., additional, Mauro, M. V., additional, Gigliotti, P., additional, Lofaro, D., additional, Greco, F., additional, Perugini, D., additional, Papalia, T., additional, Perri, A., additional, Vizza, D., additional, Giraldi, C., additional, Bonofilgio, R., additional, Luis-Lima, S., additional, Marrero, D., additional, Gonzalez-Rinne, A., additional, Torres, A., additional, Salido, E., additional, Jimenez-Sosa, A., additional, Aldea-Perona, A., additional, Gonzalez-Posada, J. M., additional, Perez-Tamajon, L., additional, Rodriguez-Hernandez, A., additional, Negrin-Mena, N., additional, Porrini, E., additional, Pihlstrom, H., additional, Dahle, D. O., additional, Holdaas, H., additional, Von Der Lippe, N., additional, Waldum, B., additional, Brekke, F., additional, Amro, A., additional, Os, I., additional, Klin, P., additional, Sanabria, H., additional, Bridoux, P., additional, De Francesco, J., additional, Fortunato, R. M., additional, Raffaele, P., additional, Kong, J., additional, Son, S. H., additional, Kwon, H. Y., additional, Whang, E. J., additional, Choi, W. Y., additional, Yoon, C. S., additional, Thanaraj, V., additional, Theakstone, A., additional, Stopper, K., additional, Ferraro, A., additional, Bhattacharjya, S., additional, Devonald, M., additional, Williams, A., additional, Mella, A., additional, Gallo, E., additional, Di Vico, M. C., additional, Pagani, F., additional, Gai, M., additional, Cho, H. J., additional, Nho, K. W., additional, Park, S.-K., additional, Kim, S. B., additional, Yoshida, K., additional, Ishii, D., additional, Ohyama, T., additional, Kohguchi, D., additional, Takeuchi, Y., additional, Varga, A., additional, Sandor, B., additional, Kalmar-Nagy, K., additional, Toth, A., additional, Toth, K., additional, Szakaly, P., additional, Kildushevsky, A., additional, Fedulkina, V., additional, Kantaria, R., additional, Staeck, O., additional, Halleck, F., additional, Rissling, O., additional, Naik, M., additional, Neumayer, H.-H., additional, Budde, K., additional, Khadzhynov, D., additional, Bhadauria, D., additional, Kaul, A., additional, Prasad, N., additional, Sharma, R. K., additional, Sezer, S., additional, Bal, Z., additional, Erkmen Uyar, M., additional, Guliyev, O., additional, Erdemir, B., additional, Colak, T., additional, Ozdemir, N., additional, Haberal, M., additional, Caliskan, Y., additional, Yazici, H., additional, Artan, A. S., additional, Oto, O. A., additional, Aysuna, N., additional, Bozfakioglu, S., additional, Turkmen, A., additional, Yildiz, A., additional, Sever, M. S., additional, Yagisawa, T., additional, Nukui, A., additional, Kimura, T., additional, Nannmoku, K., additional, Kurosawa, A., additional, Sakuma, Y., additional, Miki, A., additional, Damiano, F., additional, Ligabue, G., additional, De Biasi, S., additional, Granito, M., additional, Cossarizza, A., additional, Cappelli, G., additional, Henriques, A. C., additional, Davide, J., additional, Von During, M. E., additional, Jenssen, T. G., additional, Bollerslev, J., additional, Godang, K., additional, Asberg, A., additional, Bachelet, T., additional, Martinez, C., additional, Bello, A., additional, Kejji, S., additional, Couzi, L., additional, Guidicelli, G., additional, Lepreux, S., additional, Visentin, J., additional, Congy-Jolivet, N., additional, Rostaing, L., additional, Taupin, J.-L., additional, Kamar, N., additional, Merville, P., additional, Ozdemir, H., additional, Yildirim, S., additional, Tutal, E., additional, Sayin, B., additional, Ozdemir Acar, N., additional, Banasik, M., additional, Boratynska, M., additional, Koscielska-Kasprzak, K., additional, Kaminska, D., additional, Bartoszek, D., additional, Mazanowska, O., additional, Krajewska, M., additional, Zmonarski, S., additional, Chudoba, P., additional, Dawiskiba, T., additional, Protasiewicz, M., additional, Halon, A., additional, Sas, A., additional, Kaminska, M., additional, Klinger, M., additional, Stefanovic, N., additional, Cvetkovic, T., additional, Velickovic - Radovanovic, R., additional, Jevtovic - Stoimenov, T., additional, Vlahovic, P., additional, Rungta, R., additional, Das, P., additional, Ray, D. S., additional, Gupta, S., additional, Kolonko, A., additional, Szotowska, M., additional, Kuczera, P., additional, Chudek, J., additional, Wiecek, A., additional, Sikora-Grabka, E., additional, Adamczak, M., additional, Madej, P., additional, Amanova, A., additional, Kendi Celebi, Z., additional, Bakar, F., additional, Caglayan, M. G., additional, Keven, K., additional, Massimetti, C., additional, Imperato, G., additional, Zampi, G., additional, De Vincenzi, A., additional, Fabbri, G. D. D., additional, Brescia, F., additional, Feriozzi, S., additional, Filipov, J. J., additional, Zlatkov, B. K., additional, Dimitrov, E. P., additional, Svinarov, D. A., additional, Poesen, R., additional, De Vusser, K., additional, Evenepoel, P., additional, Kuypers, D., additional, Naesens, M., additional, Meijers, B., additional, Kocak, H., additional, Yilmaz, V. T., additional, Yilmaz, F., additional, Uslu, H. B., additional, Aliosmanoglu, I., additional, Ermis, H., additional, Dinckan, A., additional, Cetinkaya, R., additional, Ersoy, F. F., additional, Suleymanlar, G., additional, Oliveira, J.-C., additional, Santos, J., additional, Lobato, L., additional, Mendonca, D., additional, Watarai, Y., additional, Yamamoto, T., additional, Tsujita, M., additional, Hiramitsu, T., additional, Goto, N., additional, Narumi, S., additional, Kobayashi, T., additional, Line, P.-D., additional, Housawi, A., additional, House, A., additional, Ng, C., additional, Denesyk, K., additional, Rehman, F., additional, Moist, L., additional, Musetti, C., additional, Battista, M., additional, Izzo, C., additional, Guglielmetti, G., additional, Airoldi, A., additional, Stratta, P., additional, Cena, T., additional, Quaglia, M., additional, Fenoglio, R., additional, Cagna, D., additional, Amoroso, A., additional, Palmisano, A., additional, Degli Antoni, A. M., additional, Vaglio, A., additional, Piotti, G., additional, Cremaschi, E., additional, Buzio, C., additional, Maggiore, U., additional, Lee, M.-C., additional, Hsu, B.-G., additional, Zalamea Jarrin, F., additional, Sanchez Sobrino, B., additional, Lafuente Covarrubias, O., additional, Karsten Alvarez, S., additional, Dominguez Apinaniz, P., additional, Llopez Carratala, R., additional, Portoles Perez, J., additional, Yildirim, T., additional, Yilmaz, R., additional, Turkmen, E., additional, Altindal, M., additional, Arici, M., additional, Altun, B., additional, Erdem, Y., additional, Dounousi, E., additional, Mitsis, M., additional, Naka, K., additional, Pappas, H., additional, Lakkas, L., additional, Harisis, H., additional, Pappas, K., additional, Koutlas, V., additional, Tzalavra, I., additional, Spanos, G., additional, Michalis, L., additional, Siamopoulos, K., additional, Iwabuchi, T., additional, Nanmoku, K., additional, Yasunaru, S., additional, Yoshikawa, M., additional, Kitamura, K., additional, Fuji, H., additional, Fujisawa, M., additional, Nishi, S., additional, Carta, P., additional, Zanazzi, M., additional, Buti, E., additional, Larti, A., additional, Caroti, L., additional, Di Maria, L., additional, Minetti, E. E., additional, Shi, Y., additional, Luo, L., additional, Cai, B., additional, Wang, T., additional, Zou, Y., additional, Wang, L., additional, Kim, Y., additional, Kim, H. S., additional, Choi, B. S., additional, Park, C. W., additional, Yang, C. W., additional, Kim, Y.-S., additional, Chung, B. H., additional, Baek, C. H., additional, Kim, M., additional, Kim, J.-S., additional, Yang, W. S., additional, Han, D. J., additional, Mikolasevic, I., additional, Racki, S., additional, Lukenda, V., additional, Persic, M. P., additional, Colic, M., additional, Devcic, B., additional, Orlic, L., additional, Gurlek Demirci, B., additional, Say N, C. B., additional, Ozdemir Acar, F. N., additional, Vali, S., additional, Ismal, K., additional, Sahay, M., additional, Civiletti, F., additional, Cantaluppi, V., additional, Medica, D., additional, Mazzeo, A. T., additional, Assenzio, B., additional, Mastromauro, I., additional, Deambrosis, I., additional, Giaretta, F., additional, Fanelli, V., additional, Mascia, L., additional, Gkirdis, I., additional, Bechlioulis, A., additional, Evangelou, D., additional, Zarzoulas, F., additional, Kotsia, A., additional, Balafa, O., additional, Tzeltzes, G., additional, Nakas, G., additional, Kalaitzidis, R., additional, Katsouras, C., additional, Uyanik, S., additional, Toprak, S. K., additional, Ilhan, O., additional, Ekmen Uyar, M., additional, Hernandez Vargas, H., additional, Artamendi Larranaga, M., additional, Ramalle Gomara, E., additional, Gil Catalinas, F., additional, Bello Ovalle, A., additional, Pimentel Guzman, G., additional, Coloma Lopez, A., additional, Sierra Carpio, M., additional, Gil Paraiso, A., additional, Dall Anesse, C., additional, Beired Val, I., additional, Huarte Loza, E., additional, Choy, B. Y., additional, Kwan, L., additional, Mok, M., additional, Chan, T. M., additional, Yamakawa, T., additional, Kobayashi, A., additional, Yamamoto, I., additional, Mafune, A., additional, Nakada, Y., additional, Tannno, Y., additional, Tsuboi, N., additional, Yamamoto, H., additional, Yokoyama, K., additional, Ohkido, I., additional, Yokoo, T., additional, Luque, Y., additional, Anglicheau, D., additional, Rabant, M., additional, Clement, R., additional, Kreis, H., additional, Sartorius, A., additional, Noel, L.-H., additional, Timsit, M.-O., additional, Legendre, C., additional, Rancic, N., additional, Vavic, N., additional, Dragojevic-Simic, V., additional, Katic, J., additional, Jacimovic, N., additional, Kovacevic, A., additional, Mikov, M., additional, Veldhuijzen, N. M. H., additional, Rookmaaker, M. B., additional, Van Zuilen, A. D., additional, Nquyen, T. Q., additional, Boer, W. H., additional, Sahtout, W., additional, Ghezaiel, H., additional, Azzebi, A., additional, Ben Abdelkrim, S., additional, Guedri, Y., additional, Mrabet, S., additional, Nouira, S., additional, Ferdaws, S., additional, Amor, S., additional, Belarbia, A., additional, Zellama, D., additional, Mokni, M., additional, Achour, A., additional, Parikova, A., additional, Hanzal, V., additional, Fronek, J., additional, Orandi, B. J., additional, James, N. T., additional, Montgomery, R. A., additional, Desai, N. M., additional, Segev, D. L., additional, Fontana, F., additional, Ballestri, M., additional, and Magistroni, R., additional

Published
2014
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22. Characterisation of the Novel HLA-B*40:587 Allele by Sequencing-Based Typing.

Author

Blandin L, Visentin J, Cargou M, Rouzaire P, and Lemal R

Subjects
Humans, Codon, HLA-B40 Antigen genetics, Sequence Alignment, HLA-B Antigens genetics, Polymorphism, Single Nucleotide, Alleles, Exons, Histocompatibility Testing methods, Sequence Analysis, DNA methods, Base Sequence
Abstract

HLA-B*40:587 differs from HLA-B*40:02:01:01 by one nucleotide substitution in codon 275 in exon 5., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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23. Characterization of the Novel HLA-C*07:01:126 Allele by Sequencing-Based Typing.

Author

Elsermans V, Visentin J, Pajot T, Top I, and Labalette M

Subjects
Humans, Codon, Sequence Alignment, HLA-C Antigens genetics, Alleles, Exons, Histocompatibility Testing methods, Sequence Analysis, DNA methods, Base Sequence
Abstract

HLA-C*07:01:126 differs from HLA-C*07:01:01:01 by one nucleotide substitution in codon 328 in exon 7., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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24. Characterisation of the novel HLA-DPA1*01:12:03 allele by sequencing-based typing.

Author

Cargou M, Andreani M, Battarra M, Ralazamahaleo M, and Visentin J

Subjects
Humans, Codon, Sequence Alignment, HLA-DP alpha-Chains genetics, HLA-DP alpha-Chains immunology, Alleles, Exons, Histocompatibility Testing methods, Sequence Analysis, DNA methods, Base Sequence
Abstract

HLA-DPA1*01:12:03 differs from HLA-DPA1*01:12:01 by one nucleotide substitution in codon 204 in exon 4., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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25. Characterisation of the novel HLA-B*51:411 allele by sequencing-based typing.

Author

Cargou M, Elsermans V, Top I, Guidicelli G, and Visentin J

Subjects
Humans, Codon, HLA-B Antigens genetics, Sequence Alignment, Alleles, Base Sequence, Exons, Sequence Analysis, DNA methods
Abstract

HLA-B*51:411 differs from HLA-B*51:01:01:01 by one nucleotide substitution in codon 235 in exon 4., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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26. Characterisation of the novel HLA-A*26:247 allele by sequencing-based typing.

Author

Cargou M, Elsermans V, Top I, Guidicelli G, and Visentin J

Subjects
Humans, Codon, Sequence Alignment, Alleles, Base Sequence, Exons, Histocompatibility Testing methods, HLA-A Antigens genetics, Sequence Analysis, DNA methods
Abstract

HLA-A*26:247 differs from HLA-A*26:01:01:01 by one nucleotide substitution in codon 245 in exon 4., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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27. Characterisation of the novel HLA-DRB1*08:126 allele by sequencing-based typing.

Author

Elsermans V, Visentin J, Pajot T, Top I, and Labalette M

Subjects
Humans, Codon, Sequence Alignment, HLA-DRB1 Chains genetics, Alleles, Histocompatibility Testing methods, Exons, Sequence Analysis, DNA methods, Base Sequence
Abstract

HLA-DRB1*08:126 differs from HLA-DRB1*08:04:01:01 by one nucleotide substitution in codon 152 in exon 3., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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28. Characterisation of the novel HLA-DQA1*05:112 allele by sequencing-based typing.

Author

Blandin L, Visentin J, Wojciechowski E, Lemal R, and Rouzaire P

Subjects
Humans, Codon, Sequence Alignment, HLA-DQ alpha-Chains genetics, Alleles, Histocompatibility Testing methods, Exons, Sequence Analysis, DNA methods, Base Sequence
Abstract

HLA-DQA1*05:112 differs from HLA-DQA1*05:05:01:01 by one nucleotide substitution in codon -7 in exon 1., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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29. STAT expression and TFH1 cells in CVID granulomatosis and sarcoidosis: immunological and histopathological comparisons.

Author

Viallard JF, Lescure M, Oksenhendler E, Blanco P, Visentin J, and Parrens M

Subjects
Humans, Granuloma etiology, Biopsy, Signal Transduction, Common Variable Immunodeficiency complications, Sarcoidosis complications
Abstract

Granulomatous disease is a serious complication of common variable immunodeficiency (CVID-GD) that occurs in 8-22% of these patients and can mimic sarcoidosis, with which it shares certain clinical, biological, and radiological features. However, few studies to date have compared the two pathologies immunologically and histologically. Therefore, we analyzed the immunological-histological findings for different tissue samples from ten patients with CVID-GD and compared them to those of biopsy-proven sarcoidosis. Specifically, we wanted to know whether or not the signaling abnormalities observed in sarcoidosis granulomas are also present in CVID-GD. Morphological differences were found between CVID-GD histology and classical sarcoidosis: mainly, the former's notable lymphoid hyperplasia associated with granulomas not observed in the latter. All CVID-GD involved organs contained several follicular helper-T (TFH) cells within the granulomatosis, while those cells were inconstantly and more weakly expressed in sarcoidosis. Moreover, CVID and sarcoidosis granulomas expressed the phosphorylated-signal transducer and activator of transcription (pSTAT)1 and pSTAT3 factors, regardless of the organ studied and without any significant difference between entities. Our results suggest that the macrophage-activation mechanism in CVID resembles that of sarcoidosis, thereby suggesting that Janus kinase (JAK)-STAT-pathway blockade might be useful in currently difficult-to-treat CVID-GD., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Published
2024
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30. Heightened TLR7 signaling primes BCR-activated B cells in chronic graft-versus-host disease for effector functions.

Author

Bracken SJ, Suthers AN, DiCioccio RA, Su H, Anand S, Poe JC, Jia W, Visentin J, Basher F, Jordan CZ, McManigle WC, Li Z, Hakim FT, Pavletic SZ, Bhuiya NS, Ho VT, Horwitz ME, Chao NJ, and Sarantopoulos S

Subjects
Humans, Mice, Animals, Toll-Like Receptor 7 metabolism, Receptors, Antigen, B-Cell metabolism, RNA, Immunoglobulin G, Bronchiolitis Obliterans Syndrome, Nucleic Acids
Abstract

Abstract: Chronic graft-versus-host disease (cGVHD) is a debilitating, autoimmune-like syndrome that can occur after allogeneic hematopoietic stem cell transplantation. Constitutively activated B cells contribute to ongoing alloreactivity and autoreactivity in patients with cGVHD. Excessive tissue damage that occurs after transplantation exposes B cells to nucleic acids in the extracellular environment. Recognition of endogenous nucleic acids within B cells can promote pathogenic B-cell activation. Therefore, we hypothesized that cGVHD B cells aberrantly signal through RNA and DNA sensors such as Toll-like receptor 7 (TLR7) and TLR9. We found that B cells from patients and mice with cGVHD had higher expression of TLR7 than non-cGVHD B cells. Using ex vivo assays, we found that B cells from patients with cGVHD also demonstrated increased interleukin-6 production after TLR7 stimulation with R848. Low-dose B-cell receptor (BCR) stimulation augmented B-cell responses to TLR7 activation. TLR7 hyperresponsiveness in cGVHD B cells correlated with increased expression and activation of the downstream transcription factor interferon regulatory factor 5. Because RNA-containing immune complexes can activate B cells through TLR7, we used a protein microarray to identify RNA-containing antigen targets of potential pathological relevance in cGVHD. We found that many of the unique targets of active cGVHD immunoglobulin G (IgG) were nucleic acid-binding proteins. This unbiased assay identified the autoantigen and known cGVHD target Ro-52, and we found that RNA was required for IgG binding to Ro-52. Herein, we find that BCR-activated B cells have aberrant TLR7 signaling responses that promote potential effector responses in cGVHD., (Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution.)

Published
2024
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31. Characterization of the novel HLA-C*05:286 allele by sequencing-based typing.

Author

Cargou M, Elsermans V, Top I, Duclaut M, and Visentin J

Subjects
Humans, Alleles, Histocompatibility Testing, Codon, Sequence Analysis, DNA, HLA-C Antigens genetics, Genes, MHC Class I
Abstract

HLA-C*05:286 differs from HLA-C*05:01:01:02 by one nucleotide substitution in codon 283 in exon 5., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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32. 25-hydroxyvitamin D sufficiency is associated with lower de novo anti-HLA donor specific antibody and better kidney transplant outcomes.

Author

Bakis H, Bouthemy C, Corcuff JB, Lauro C, Guidicelli G, Cargou M, Guibet C, Taton B, Merville P, Couzi L, Moreau K, and Visentin J

Subjects
Humans, Retrospective Studies, Risk Factors, HLA Antigens, Alleles, Antibodies, Graft Rejection, Isoantibodies, Kidney Transplantation, Vitamin D analogs & derivatives
Abstract

T-cell mediated rejection (TCMR), de novo anti-HLA donor-specific antibodies (dnDSAs) and ensuing antibody-mediated rejection (ABMR) reduce kidney transplantation (KT) survival. The immunomodulatory effects of 25-hydroxyvitamin D [25(OH)D] could be beneficial for KT outcomes. We aimed to evaluating the association between 25(OH)D levels, the development of dnDSAs, clinical TCMR and ABMR, and graft survival. This single center retrospective study included 253 KT recipients (KTRs) transplanted without preformed DSA between 2010 and 2013. We measured 25(OH)D in successive serum samples: at KT (M0) and M12 for the entire cohort, and additionally at M24 and/or M36 when sera were available. We assessed graft outcomes up to 5 years post-KT. The proportion of KTRs having sufficient 25(OH)D at KT (M0) was high (81.4%) and then dropped at M12 (71.1%). KTRs with sufficient 25(OH)D at M0 experienced less clinical TCMR (HR, 0.41; 95% CI, 0.19-0.88 in multivariate analysis). A sufficient 25(OH)D at M12 was independently associated with a longer dnDSA-free survival (HR, 0.34; 95% CI, 0.17-0.69). There was no association between 25(OH)D and clinical AMBR. Studying the KTRs with 25(OH)D measurements at M12, M24 and M36 (n = 203), we showed that 25(OH)D sufficiency over the 3 first-years post-KT was associated with a longer graft survival in multivariate analyses (HR, 0.39; 95% CI, 0.22-0.70). To our knowledge, this study is the first showing an association between 25(OH)D sufficiency post-KT and dnDSA occurrence in KTRs. Moreover, we reinforce previously published data showing an association between 25(OH)D, TCMR and graft survival in KT., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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33. Characterization of the novel HLA-C*16:98:02 allele by sequencing-based typing.

Author

Blandin L, Visentin J, Duclaut M, Lemal R, and Rouzaire P

Subjects
Humans, Alleles, Histocompatibility Testing, Codon, Sequence Analysis, DNA, HLA-C Antigens genetics, Genes, MHC Class I
Abstract

HLA-C*16:98:02 differs from HLA-C*16:98:01 by one nucleotide substitution in codon 132 in exon 3., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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34. Characterization of the novel HLA-B*40:539 allele by sequencing-based typing.

Author

Elsermans V, Visentin J, Top I, Pajot T, and Labalette M

Subjects
Humans, Alleles, Histocompatibility Testing, Codon, Sequence Analysis, DNA, Genes, MHC Class I, HLA-B Antigens genetics
Abstract

HLA-B*40:539 differs from HLA-B*40:01:01 by one nucleotide substitution in codon 46 in exon 2., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2024
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35. Characterization of the novel HLA-DRB1*11:01:01:12N allele by sequencing-based typing.

Author

Cargou M, Elsermans V, Cambridge CA, Lasseaux E, and Visentin J

Subjects
Humans, HLA-DRB1 Chains genetics, Base Sequence, Alleles, Sequence Analysis, DNA, Nucleotides
Abstract

HLA-DRB1*11:01:01:12N differs from HLA-DRB1*11:01:01:03 by one nucleotide substitution in intron 3 at position c.652+1G>C, hg19., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2023
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36. Measurement of the Immunosuppressant Possession Ratio by Transplant Clinical Pharmacists Captures a Non-Adherence Associated With Antibody-Mediated Rejection.

Author

Chambord J, Chauveau B, Djabarouti S, Vignaud J, Taton B, Moreau K, Visentin J, Merville P, Xuereb F, and Couzi L

Subjects
Humans, Case-Control Studies, Pharmacists, Antibodies, Graft Rejection prevention & control, Graft Rejection diagnosis, Isoantibodies, Immunosuppressive Agents therapeutic use, Kidney Transplantation
Abstract

Our objective was to calculate an immunosuppressant possession ratio (IPR) to diagnose non-adherence at the time of antibody-mediated rejection (ABMR). IPR was defined as the ratio of number of pills collected at the pharmacy to the number of pills prescribed over a defined period. In a first cohort of 91 kidney transplant recipients (KTRs), those with an IPR < 90% had more frequently a tacrolimus through level coefficient of variation >30% than patients with an IPR = 100% (66.7% vs. 29.4%, p = 0.05). In a case-control study, 26 KTRs with ABMR had lower 6 months IPRs than 26 controls (76% vs. 99%, p < 0.001). In KTRs with ABMR, non-adherence was more often diagnosed by a 6 months IPR < 90% than by clinical suspicion (73.1% vs 30.8%, p = 0.02). In the multivariable analysis, only de novo DSA and 6 months IPR < 90% were independently associated with ABMR, whereas clinical suspicion was not (odds ratio, 4.73; 95% CI, 1.17-21.88; p = 0.03; and odds ratio, 6.34; 95% CI, 1.73-25.59; p = 0.007, respectively). In summary, IPR < 90% is a quantifiable tool to measure immunosuppressant non-adherence. It is better associated with ABMR than clinical suspicion of non-adherence., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Chambord, Chauveau, Djabarouti, Vignaud, Taton, Moreau, Visentin, Merville, Xuereb and Couzi.)

Published
2023
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37. Impact of Preformed Donor-Specific Anti-HLA-Cw and Anti-HLA-DP Antibodies on Acute Antibody-Mediated Rejection in Kidney Transplantation.

Author

Laboux T, Lenain R, Visentin J, Flahaut G, Chamley P, Provôt F, Top I, Kerleau C, Labalette M, Choukroun G, Couzi L, Blancho G, Hazzan M, and Maanaoui M

Subjects
Humans, Antibodies, Graft Rejection, Graft Survival, Histocompatibility Testing, HLA Antigens, Tissue Donors, Kidney Transplantation adverse effects
Abstract

Given the risk of rejection, the presence of preformed donor specific antibodies (DSA) contraindicates transplantation in most allocation systems. However, HLA-Cw and -DP DSA escape this censorship. We performed a multicentric observational study, in which the objective was to determinate risk factors of acute antibody-mediated rejection (aABMR) in recipients transplanted with preformed isolated Cw- or DP-DSA. Between 2010 and 2019, 183 patients were transplanted with a preformed isolated Cw- or DP-DSA (92 Cw-DSA; 91 DP-DSA). At 2 years, the incidence of aABMR was 12% in the Cw-DSA group, versus 28% in the DP-DSA group. Using multivariable Cox regression model, the presence of a preformed DP-DSA was associated with an increased risk of aABMR (HR = 2.32 [1.21-4.45 ( p = 0.001)]) compared with Cw-DSA. We also observed a significant association between the DSA's MFI on the day of transplant and the risk of aABMR (HR = 1.09 [1.08-1.18], p = 0.032), whatever the DSA was. Interaction term analysis found an increased risk of aABMR in the DP-DSA group compared with Cw-DSA, but only for MFI below 3,000. These results may plead for taking these antibodies into account in the allocation algorithms, in the same way as other DSA., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Laboux, Lenain, Visentin, Flahaut, Chamley, Provôt, Top, Kerleau, Labalette, Choukroun, Couzi, Blancho, Hazzan and Maanaoui.)

Published
2023
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40. Characterization of the novel HLA-C*12:384 allele by sequencing-based typing.

Author

Cargou M, Elsermans V, Top I, Wojciechowski E, and Visentin J

Subjects
Humans, Alleles, Histocompatibility Testing, Codon, Sequence Analysis, DNA, HLA-C Antigens genetics, Genes, MHC Class I
Abstract

HLA-C*12:384 differs from HLA-C*12:03:01:02 by one nucleotide substitution in codon 42 in exon 2., (© 2023 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

Published
2023
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41. Characterization of the novel HLA-DPA1*02:115 allele by sequencing-based typing.

Author

Blandin L, Visentin J, Cargou M, Lemal R, and Rouzaire P

Subjects
Humans, Alleles, Sequence Alignment, Histocompatibility Testing, Sequence Analysis, DNA, HLA-DP alpha-Chains genetics
Abstract

HLA-DPA1*02:115 differs from HLA-DPA1*02:01:01:06 by one nucleotide substitution in codon 224 in exon 4., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2023
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42. Characterization of the novel HLA-B*44:324:02 allele by sequencing-based typing.

Author

Cargou M, Elsermans V, Top I, Guidicelli G, and Visentin J

Subjects
Humans, Alleles, Histocompatibility Testing, Codon, Sequence Analysis, DNA, HLA-B Antigens
Abstract

HLA-B*44:324:02 differs from HLA-B*44:324:01 by one nucleotide substitution in codon 99 in exon 3., (© 2023 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

Published
2023
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43. Characterization of the novel HLA-A*24:587 allele by sequencing-based typing.

Author

Cargou M, Elsermans V, Top I, Wojciechowski E, and Visentin J

Subjects
Humans, Alleles, Histocompatibility Testing, Codon, Sequence Analysis, DNA, HLA-A Antigens genetics
Abstract

HLA-A*24:587 differs from HLA-A*24:02:01:01 by one nucleotide substitution in codon 220 in exon 4., (© 2023 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

Published
2023
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44. Characterization of the novel HLA-C*03:552 allele by sequencing-based typing.

Author

Elsermans V, Visentin J, Top I, Pajot T, and Labalette M

Subjects
Humans, Alleles, Histocompatibility Testing, Codon, HLA-C Antigens genetics, Genes, MHC Class I
Abstract

HLA-C*03:552 differs from HLA-C*03:04:01:01 by one nucleotide substitution in codon 72 in exon 2., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2023
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45. Single-cell landscape analysis unravels molecular programming of the human B cell compartment in chronic GVHD.

Author

Poe JC, Fang J, Zhang D, Lee MR, DiCioccio RA, Su H, Qin X, Zhang JY, Visentin J, Bracken SJ, Ho VT, Wang KS, Rose JJ, Pavletic SZ, Hakim FT, Jia W, Suthers AN, Curry-Chisolm IM, Horwitz ME, Rizzieri DA, McManigle WC, Chao NJ, Cardones AR, Xie J, Owzar K, and Sarantopoulos S

Subjects
Humans, B-Lymphocytes, Receptors, Antigen, B-Cell genetics, Graft vs Host Disease, Hematopoietic Stem Cell Transplantation adverse effects, Bronchiolitis Obliterans Syndrome
Abstract

Alloreactivity can drive autoimmune syndromes. After allogeneic hematopoietic stem cell transplantation (allo-HCT), chronic graft-versus-host disease (cGVHD), a B cell-associated autoimmune-like syndrome, commonly occurs. Because donor-derived B cells continually develop under selective pressure from host alloantigens, aberrant B cell receptor (BCR) activation and IgG production can emerge and contribute to cGVHD pathobiology. To better understand molecular programing of B cells in allo-HCT, we performed scRNA-Seq analysis on high numbers of purified B cells from patients. An unsupervised analysis revealed 10 clusters, distinguishable by signature genes for maturation, activation, and memory. Within the memory B cell compartment, we found striking transcriptional differences in allo-HCT patients compared with healthy or infected individuals, including potentially pathogenic atypical B cells (ABCs) that were expanded in active cGVHD. To identify intrinsic alterations in potentially pathological B cells, we interrogated all clusters for differentially expressed genes (DEGs) in active cGVHD versus patients who never had signs of immune tolerance loss (no cGVHD). Active cGVHD DEGs occurred in both naive and BCR-activated B cell clusters. Remarkably, some DEGs occurred across most clusters, suggesting common molecular programs that may promote B cell plasticity. Our study of human allo-HCT and cGVHD provides understanding of altered B cell memory during chronic alloantigen stimulation.

Published
2023
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46. Characterization of the novel HLA-C*17:01:18 allele by sequencing-based typing.

Author

Cargou M, Elsermans V, Top I, Wojciechowski E, and Visentin J

Subjects
Humans, Alleles, Histocompatibility Testing, Sequence Analysis, DNA, Exons genetics, HLA-C Antigens genetics
Abstract

HLA-C*17:01:18 differs from HLA-C*17:01:01:05 by one nucleotide substitution in codon 18 in exon 2., (© 2022 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

Published
2022
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47. Characterization of the novel HLA-C*07:1023 allele by sequencing-based typing.

Author

Blandin L, Visentin J, Guidicelli G, Rouzaire P, and Lemal R

Subjects
Humans, Alleles, Histocompatibility Testing, Sequence Analysis, DNA, Exons genetics, HLA-C Antigens genetics
Abstract

HLA-C*07:1023 differs from HLA-C*07:01:01:01 by one nucleotide substitution in codon 313 in exon 5., (© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2022
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48. Characterization of the novel HLA-DQA1*01:89 allele by sequencing-based typing.

Author

Cargou M, Andreani M, Bianculli AG, Guidicelli G, and Visentin J

Subjects
Humans, HLA-DQ alpha-Chains genetics, Sequence Analysis, DNA, Exons genetics, Alleles
Abstract

HLA-DQA1*01:89 differs from HLA-DQA1*01:01:01:01 by one nucleotide substitution in codon -5 in exon 1., (© 2022 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

Published
2022
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49. Characterization of the novel HLA-A*01:419 allele by sequencing-based typing.

Author

Blandin L, Visentin J, Ralazamahaleo M, Lemal R, and Rouzaire P

Subjects
Humans, Alleles, Histocompatibility Testing, Sequence Analysis, DNA, Exons genetics, HLA-A Antigens genetics
Abstract

HLA-A*01:419 differs from HLA-A*01:01:01:03 by one nucleotide substitution in codon 200 in exon 4., (© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Published
2022
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50. Characterization of the novel HLA-A*11:422 allele by sequencing-based typing.

Author

Cargou M, Elsermans V, Top I, Blandin L, and Visentin J

Subjects
Humans, Alleles, Histocompatibility Testing, Sequence Analysis, DNA, Exons genetics, HLA-A Antigens genetics
Abstract

HLA-A*11:422 differs from HLA-A*11:01:01:01 by one nucleotide substitution in codon 285 in exon 5., (© 2022 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

Published
2022
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