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Start Over Author "Anne M. Stevens" Journal clinical immunology
5 results on '"Anne M. Stevens"'

1. Altered signaling in systemic juvenile idiopathic arthritis monocytes

Author

Justin Lee, Claudia Macaubas, Yujuan Zhang, Diana Milojevic, Anne M. Stevens, Vivian E. Saper, Norman T. Ilowite, Elizabeth Wong, Khoa D. Nguyen, Elizabeth D. Mellins, Tzielan Lee, and Susan Shenoi

Subjects
Male, 0301 basic medicine, Adolescent, Immunology, Arthritis, Suppressor of Cytokine Signaling Proteins, Real-Time Polymerase Chain Reaction, Systemic inflammation, Monocytes, Article, Pathogenesis, Interferon-gamma, Young Adult, 03 medical and health sciences, Suppressor of Cytokine Signaling 1 Protein, 0302 clinical medicine, medicine, Humans, Immunology and Allergy, Interferon gamma, STAT1, Phosphorylation, Child, 030203 arthritis & rheumatology, biology, Reverse Transcriptase Polymerase Chain Reaction, Suppressor of cytokine signaling 1, Infant, Flow Cytometry, medicine.disease, Arthritis, Juvenile, STAT1 Transcription Factor, 030104 developmental biology, Gene Expression Regulation, Case-Control Studies, Child, Preschool, biology.protein, Female, Interferons, Signal transduction, medicine.symptom, Signal Transduction, medicine.drug
Abstract

Systemic juvenile idiopathic arthritis (sJIA) is characterized by systemic inflammation and arthritis. Monocytes are implicated in sJIA pathogenesis, but their role in disease is unclear. The response of sJIA monocytes to IFN may be dysregulated. We examined intracellular signaling in response to IFN type I (IFNα) and type II (IFNγ) in monocytes during sJIA activity and quiescence, in 2 patient groups. Independent of disease activity, monocytes from Group 1 (collected between 2002 and 2009) showed defective STAT1 phosphorylation downstream of IFNs, and expressed higher transcript levels of SOCS1, an inhibitor of IFN signaling. In the Group 2 (collected between 2011 and 2014), monocytes of patients with recent disease onset were IFNγ hyporesponsive, but in treated, quiescent subjects, monocytes were hyperresponsive to IFNγ. Recent changes in medication in sJIA may alter the IFN hyporesponsiveness. Impaired IFN/pSTAT1 signaling is consistent with skewing of sJIA monocytes away from an M1 phenotype and may contribute to disease pathology.

Published
2016
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2. Genetic associations of leptin-related polymorphisms with systemic lupus erythematosus

Author

Marta E. Alarcón-Riquelme, Ignacio García-De La Torre, Luis J. Catoggio, Timothy B. Niewold, Ana I. Marcos, Barry I. Freedman, Pilar C. Marino, Marisa Jorfen, Griselda Buchanan, Marcelo Abdala, Anne M. Stevens, Fernando A. Ramos, Emoke Endreffy, Sandra M. Navarro, Ana M. Bertoli, Sergio Migliarese, Jorge Manni, Jose L. Presas, César Graf, László Kovács, Hye jin Jeong, John B. Harley, Berta Martins da Silva, Cesar Caprarulo, Guillermo Tate, Jennifer M. Grossman, Julio Sánchez-Román, Jian Zhao, Javier Martin, Cristina G. Battagliotti, Estela Bertero, Chaim O. Jacob, Carlos E. Perandones, Kenneth M. Kaufman, Guillermo A. Berbotto, Alberto Allievi, John D. Reveille, Sebastian Grimaudo, Estela L. Motta, Susana Gamron, Yeong Wook Song, Mario Cardiel Ríos, José Luis Callejas, Gary S. Gilkeson, Mercedes A. García, Hugo R. Scherbarth, Kathy Moser Sivils, María Francisca González-Escribano, Alejandro Alvarellos, Antonio La Cava, Mariano Cucho, Joan T. Merrill, Carlos D. Santos, Torsten Witte, Cristina Drenkard, R. Hal Scofield, Seung Taek Song, Cristina Prigione, Lindsey A. Criswell, Mariela Bearzotti, Deh Ming Chang, José Mario Sabio, Francisco Caeiro, Mauro Galeazzi, Rosalind Ramsey-Goldman, Simon A. Palatnik, Lennart Truedsson, Marco Maradiaga Ceceña, Johan Frostegård, Susan A. Boackle, Sanatorio Parque, Francisco Moctezuma, Hui Wu, Juan Carlos Marcos, Eduardo Acevedo, Timothy J. Vyse, Jennifer A. Kelly, Michelle Petri, Carlos Vasconcelos, Sandra D'Alfonso, Elizabeth E. Brown, Norberto Ortego-Centeno, Betty P. Tsao, Enrique de Ramón, Juan-Manuel Anaya, Diane L. Kamen, Emilia Menso, Gian Domenico Sebastiani, Patrick M. Gaffney, Judith A. James, Sang Cheol Bae, Susana Roverano, Carolina Guillerón, Jeffrey C. Edberg, Enrique R. Soriano, Carl D. Langefeld, Elisa J. Romero, Alicia Eimon, Bevra H. Hahn, Robert P. Kimberly, Luis M. Vilá, Graciela S. Alarcón, Sergio Paira, Bernard Lauwerys, Zhao, J., Wu, H., Langefeld, C. D., Kaufman, K. M., Kelly, J. A., Bae, S. -C., Alarcon-Riquelme, M. E., Alarcon, G. S., Anaya, J. -M., Criswell, L. A., Freedman, B. I., Kamen, D. L., Gilkeson, G. S., Jacob, C. O., James, J. A., Merrill, J. T., Gaffney, P. M., Sivils, K. M., Niewold, T. B., Petri, M. A., Song, S. T., Jeong, H. -J., Ramsey-Goldman, R., Reveille, J. D., Hal Scofield, R., Stevens, A. M., Boackle, S. A., Vila, L. M., Chang, D. -M., Song, Y. W., Vyse, T. J., Harley, J. B., Brown, E. E., Edberg, J. C., Kimberly, R. P., Hahn, B. H., Grossman, J. M., Tsao, B. P., La Cava, A., Frostegard, J., Truedsson, L., de Ramon, E., Sabio, J. M., Gonzalez-Escribano, M. F., Martin, J., Ortego-Centeno, N., Callejas, J. L., Sanchez-Roman, J., D'Alfonso, S., Migliarese, S., Sebastiani, G. -D., Galeazzi, M., Witte, T., Lauwerys, B. R., Endreffy, E., Kovacs, L., Vasconcelos, C., da Silva, B. M., Scherbarth, H. R., Marino, P. C., Motta, E. L., Gamron, S., Drenkard, C., Menso, E., Allievi, A., Tate, G. A., Presas, J. L., Palatnik, S. A., Abdala, M., Bearzotti, M., Alvarellos, A., Caeiro, F., Bertoli, A., Paira, S., Roverano, S., Graf, C. E., Bertero, E., Caprarulo, C., Buchanan, G., Guilleron, C., Grimaudo, S., Manni, J., Catoggio, L. J., Soriano, E. R., Santos, C. D., Prigione, C., Ramos, F. A., Navarro, S. M., Berbotto, G. A., Jorfen, M., Romero, E. J., Garcia, M. A., Marcos, J. C., Marcos, A. I., Perandones, C. E., Eimon, A., Parque, S., Battagliotti, C. G., Acevedo, E., Cucho, M., de la Torre, I. G., Rios, M. C., Moctezuma, F., and Maradiaga Cecena, M.

Subjects
Leptin, Hispanic, Gene, Dna determination, immune system diseases, Lep gene, Genotype, 2.1 Biological and endogenous factors, Lupus Erythematosus, Systemic, Immunology and Allergy, Medicine, Aetiology, skin and connective tissue diseases, Priority journal, Leptin pathway, Gene polymorphism, Gene polymorphisms, Single Nucleotide, East asian, Case-Control Studie, Human, Lepr gene, Immunology, Case control study, Lupus, Single-nucleotide polymorphism, Major clinical study, Systemic lupus erythematosu, Autoimmune Disease, Polymorphism, Single Nucleotide, Article, European american, Systemic lupus erythematosus, Clinical Research, Genetic susceptibility, Genetics, Genetic predisposition, Humans, Genetic Predisposition to Disease, Genetic Testing, African american, Polymorphism, Genetic risk, Inflammation, Lupus Erythematosus, business.industry, Inflammatory and immune system, Pparg gene, Marta E. Alarcón-Riquelme for the BIOLUPUS and GENLES networks, Systemic, Case-control study, Single nucleotide polymorphism, Case-Control Studies, Multiple comparisons problem, Genetic association, Ghsr gene, business, Controlled study
Abstract

Leptin is abnormally elevated in the plasma of patients with systemic lupus erythematosus (SLE), where it is thought to promote and/or sustain pro-inflammatory responses. Whether this association could reflect an increased genetic susceptibility to develop SLE is not known, and studies of genetic associations with leptin-related polymorphisms in SLE patients have been so far inconclusive. Here we genotyped DNA samples from 15,706 SLE patients and healthy matched controls from four different ancestral groups, to correlate polymorphisms of genes of the leptin pathway to risk for SLE. It was found that although several SNPs showed weak associations, those associations did not remain significant after correction for multiple testing. These data do not support associations between defined leptin-related polymorphisms and increased susceptibility to develop SLE. © 2015 Elsevier Inc.

Published
2015
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