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1. Corrigendum: The paradigm of IL-23-independent production of IL-17F and IL-17A and their role in chronic inflammatory diseases

Author

Navarro-Compán, Victoria, primary, Puig, Luis, additional, Vidal, Silvia, additional, Ramírez, Julio, additional, Llamas-Velasco, Mar, additional, Fernández-Carballido, Cristina, additional, Almodóvar, Raquel, additional, Pinto, José Antonio, additional, Galíndez-Aguirregoikoa, Eva, additional, Zarco, Pedro, additional, Joven, Beatriz, additional, Gratacós, Jordi, additional, Juanola, Xavier, additional, Blanco, Ricardo, additional, Arias-Santiago, Salvador, additional, Sanz, Jesús Sanz, additional, Queiro, Rubén, additional, and Cañete, Juan D., additional

Published
2023
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2. The paradigm of IL-23-independent production of IL-17F and IL-17A and their role in chronic inflammatory diseases

Author

Navarro-Compán, Victoria, primary, Puig, Luis, additional, Vidal, Silvia, additional, Ramírez, Julio, additional, Llamas-Velasco, Mar, additional, Fernández-Carballido, Cristina, additional, Almodóvar, Raquel, additional, Pinto, José Antonio, additional, Galíndez-Aguirregoikoa, Eva, additional, Zarco, Pedro, additional, Joven, Beatriz, additional, Gratacós, Jordi, additional, Juanola, Xavier, additional, Blanco, Ricardo, additional, Arias-Santiago, Salvador, additional, Sanz Sanz, Jesús, additional, Queiro, Rubén, additional, and Cañete, Juan D., additional

Published
2023
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3. Brief Report: Association of HLA–DRB1*01 With IgA Vasculitis (Henoch-Schönlein)

Author

López-Mejías, Raquel, Genre, Fernanda, Pérez, Belén Sevilla, Castañeda, Santos, Ortego-Centeno, Norberto, Llorca, Javier, Ubilla, Begoña, Remuzgo-Martínez, Sara, Mijares, Verónica, Pina, Trinitario, Calvo-Río, Vanesa, Márquez, Ana, Sala-Icardo, Luis, Miranda-Filloy, José A., Conde-Jaldón, Marta, Ortiz-Fernández, Lourdes, Rubio, Esteban, Luque, Manuel León, Blanco-Madrigal, Juan M., Galíndez-Aguirregoikoa, Eva, González-Vela, Carmen M., Ocejo-Vinyals, Gonzalo J., Escribano, Francisca González, Martín, Javier, Blanco, Ricardo, and González-Gay, Miguel A.

Published
2015
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5. A genome-wide association study suggests the HLA Class II region as the major susceptibility locus for IgA vasculitis

Author

López-Mejías, Raquel, primary, Carmona, F. David, additional, Castañeda, Santos, additional, Genre, Fernanda, additional, Remuzgo-Martínez, Sara, additional, Sevilla-Perez, Belén, additional, Ortego-Centeno, Norberto, additional, Llorca, Javier, additional, Ubilla, Begoña, additional, Mijares, Verónica, additional, Pina, Trinitario, additional, Miranda-Filloy, José A., additional, Navas Parejo, Antonio, additional, de Argila, Diego, additional, Aragües, Maximiliano, additional, Rubio, Esteban, additional, Luque, Manuel León, additional, Blanco-Madrigal, Juan María, additional, Galíndez-Aguirregoikoa, Eva, additional, Jayne, David, additional, Blanco, Ricardo, additional, Martín, Javier, additional, and González-Gay, Miguel A., additional

Published
2017
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6. Additional file 1: Table S1. of Role of PTPN22 and CSK gene polymorphisms as predictors of susceptibility and clinical heterogeneity in patients with Henoch-Schönlein purpura (IgA vasculitis)

Author

López-Mejías, Raquel, Genre, Fernanda, Remuzgo-Martínez, Sara, Pérez, Belén, Castañeda, Santos, Llorca, Javier, Ortego-Centeno, Norberto, Ubilla, Begoña, Mijares, Verónica, Trinitario Pina, Calvo-Río, Vanesa, Palmou, Natalia, Miranda-Filloy, José, Parejo, Antonio, Argila, Diego, Sánchez-Pérez, Javier, Rubio, Esteban, Luque, Manuel, Blanco-Madrigal, Juan, Galíndez-Aguirregoikoa, Eva, J. Ocejo-Vinyals, Martín, Javier, Blanco, Ricardo, and González-Gay, Miguel

Abstract

Different genetic models of inheritance for CSK polymorphisms. (DOC 28 kb)

Published
2015
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7. Additional file 2: Table S2. of Role of PTPN22 and CSK gene polymorphisms as predictors of susceptibility and clinical heterogeneity in patients with Henoch-Schönlein purpura (IgA vasculitis)

Author

López-Mejías, Raquel, Genre, Fernanda, Remuzgo-Martínez, Sara, Pérez, Belén, Castañeda, Santos, Llorca, Javier, Ortego-Centeno, Norberto, Ubilla, Begoña, Mijares, Verónica, Trinitario Pina, Calvo-Río, Vanesa, Palmou, Natalia, Miranda-Filloy, José, Parejo, Antonio, Argila, Diego, Sánchez-Pérez, Javier, Rubio, Esteban, Luque, Manuel, Blanco-Madrigal, Juan, Galíndez-Aguirregoikoa, Eva, J. Ocejo-Vinyals, Martín, Javier, Blanco, Ricardo, and González-Gay, Miguel

Abstract

CSK and PTPN22 haplotype analysis. (DOC 33 kb)

Published
2015
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8. Additional file 3: Table S3. of Role of PTPN22 and CSK gene polymorphisms as predictors of susceptibility and clinical heterogeneity in patients with Henoch-Schönlein purpura (IgA vasculitis)

Author

López-Mejías, Raquel, Genre, Fernanda, Remuzgo-Martínez, Sara, Pérez, Belén, Castañeda, Santos, Llorca, Javier, Ortego-Centeno, Norberto, Ubilla, Begoña, Mijares, Verónica, Trinitario Pina, Calvo-Río, Vanesa, Palmou, Natalia, Miranda-Filloy, José, Parejo, Antonio, Argila, Diego, Sánchez-Pérez, Javier, Rubio, Esteban, Luque, Manuel, Blanco-Madrigal, Juan, Galíndez-Aguirregoikoa, Eva, J. Ocejo-Vinyals, Martín, Javier, Blanco, Ricardo, and González-Gay, Miguel

Subjects
musculoskeletal diseases, skin and connective tissue diseases
Abstract

Genotype and allele frequencies of CSK and PTPN22 gene polymorphisms in HSP patients according to sex and the presence of joint manifestations (arthralgia or arthritis). (DOC 67 kb)

Published
2015
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9. Role of PTPN22 and CSK gene polymorphisms as predictors of susceptibility and clinical heterogeneity in patients with Henoch-Schönlein purpura (IgA vasculitis)

Author

López-Mejías, Raquel, primary, Genre, Fernanda, additional, Remuzgo-Martínez, Sara, additional, Pérez, Belén Sevilla, additional, Castañeda, Santos, additional, Llorca, Javier, additional, Ortego-Centeno, Norberto, additional, Ubilla, Begoña, additional, Mijares, Verónica, additional, Pina, Trinitario, additional, Calvo-Río, Vanesa, additional, Palmou, Natalia, additional, Miranda-Filloy, José A., additional, Parejo, Antonio Navas, additional, Argila, Diego, additional, Sánchez-Pérez, Javier, additional, Rubio, Esteban, additional, Luque, Manuel León, additional, Blanco-Madrigal, Juan María, additional, Galíndez-Aguirregoikoa, Eva, additional, Ocejo-Vinyals, J. Gonzalo, additional, Martín, Javier, additional, Blanco, Ricardo, additional, and González-Gay, Miguel A., additional

Published
2015
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10. Association of HLA-B*41:02 with Henoch-Schönlein Purpura (IgA Vasculitis) in Spanish individuals irrespective of the HLA-DRB1 status

Author

López-Mejías, Raquel, primary, Genre, Fernanda, additional, Pérez, Belén Sevilla, additional, Castañeda, Santos, additional, Ortego-Centeno, Norberto, additional, Llorca, Javier, additional, Ubilla, Begoña, additional, Remuzgo-Martínez, Sara, additional, Mijares, Verónica, additional, Pina, Trinitario, additional, Calvo-Río, Vanesa, additional, Márquez, Ana, additional, Miranda-Filloy, José A, additional, Parejo, Antonio Navas, additional, Conde-Jaldón, Marta, additional, Ortiz-Fernández, Lourdes, additional, Argila, Diego, additional, Aragües, Maximiliano, additional, Rubio, Esteban, additional, León Luque, Manuel, additional, Blanco-Madrigal, Juan María, additional, Galíndez-Aguirregoikoa, Eva, additional, Escribano, Francisca González, additional, Ocejo-Vinyals, J Gonzalo, additional, Martín, Javier, additional, Blanco, Ricardo, additional, and González-Gay, Miguel A, additional

Published
2015
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11. Role of PTPN22and CSKgene polymorphisms as predictors of susceptibility and clinical heterogeneity in patients with Henoch-Schönlein purpura (IgA vasculitis)

Author

López-Mejías, Raquel, Genre, Fernanda, Remuzgo-Martínez, Sara, Pérez, Belén, Castañeda, Santos, Llorca, Javier, Ortego-Centeno, Norberto, Ubilla, Begoña, Mijares, Verónica, Pina, Trinitario, Calvo-Río, Vanesa, Palmou, Natalia, Miranda-Filloy, José, Parejo, Antonio, Argila, Diego, Sánchez-Pérez, Javier, Rubio, Esteban, Luque, Manuel, Blanco-Madrigal, Juan, Galíndez-Aguirregoikoa, Eva, Ocejo-Vinyals, J., Martín, Javier, Blanco, Ricardo, and González-Gay, Miguel

Abstract

To determine whether the PTPN22 (protein tyrosine phosphatase nonreceptor 22)/CSK (c-src tyrosine kinase) pathway is implicated in the susceptibility and clinical heterogeneity of Henoch-Schönlein purpura (HSP) in the largest series of Caucasian HSP patients ever assessed for genetic studies. A set of 329 Spanish patients diagnosed with HSP fulfilling the American College of Rheumatology and the Michel et al. classification criteria and 515 sex and ethnically matched controls were recruited in this study. Two well-known CSK(CSKrs34933034 and CSKrs1378942) and two functional PTPN22(PTPN22rs2476601 (R620W) and PTPN22rs33996649 (R263Q)) polymorphisms, previously associated with autoimmunity, were genotyped with TaqMan single nucleotide polymorphism (SNP) genotyping assays. No significant differences in the genotype and allele frequencies between HSP patients and controls were observed when the CSKrs34933034, CSKrs1378942, PTPN22rs2476601 (R620W) and PTPN22rs33996649 (R263Q) polymorphisms were analyzed independently. In keeping with this observation, no significant differences were found when we assessed these polymorphisms combined conforming haplotypes. In addition, there were no differences in the allele or genotype frequencies when HSP patients were stratified according the age at disease onset, sex, presence of arthralgia/arthritis, nephritis or gastrointestinal manifestations. Our results do not support association between PTPN22/CSKand HSP.

Published
2015
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12. Interleukin 1 beta (IL1ß) rs16944 genetic variant as a genetic marker of severe renal manifestations and renal sequelae in Henoch-Schönlein purpura.

Author

López-Mejías R, Genre F, Remuzgo-Martínez S, Sevilla Pérez B, Castañeda S, Llorca J, Ortego-Centeno N, Ubilla B, Mijares V, Pina T, Calvo-Río V, Miranda-Filloy JA, Navas Parejo A, Argila D, Sánchez-Pérez J, Rubio E, Luque ML, Blanco-Madrigal JM, Galíndez-Aguirregoikoa E, Martín J, Blanco R, and González-Gay MA

Subjects
Adolescent, Child, Child, Preschool, Female, Genetic Markers genetics, Genotype, Humans, IgA Vasculitis complications, Male, IgA Vasculitis genetics, Interleukin-1beta genetics, Kidney Diseases etiology, Polymorphism, Single Nucleotide
Abstract

Objectives: Data from a small series suggested that the Interleukin 1 beta (IL1ß) rs16944 polymorphism may be associated with severe renal involvement and persistent renal damage (renal sequelae) in Henoch-Schönlein purpura (HSP). To confirm this association, we assessed the largest cohort of Caucasian HSP patients ever considered for genetic studies., Methods: 338 Spanish HSP patients and 635 sex and ethnically matched controls were recruited in this study. All patients were required to have had at least 6 months' follow-up. Patients and controls were genotyped for IL1β rs16944 by TaqMan genotyping assay., Results: No differences between IL1β rs16944 genotype or allele frequencies were found either in the case/control study or when HSP patients were stratified according to the age at disease onset, presence of nephritis or gastrointestinal manifestations. Nevertheless, 4 (25%) of the 16 HSP patients who developed severe renal manifestations carried the TT genotype versus 29 (9%) of 322 who did not develop this complication (p=0.01, OR=5.48, 95% CI: 1.01-28.10). Accordingly, patients carrying the mutant T allele had an increased risk of developing severe nephropathy (p=0.016, OR=2.35, 95% CI: 1.09-5.07). Additionally, a significant increase of the TT genotype was observed in patients with persistent renal damage when compared with those patients without this complication (25% versus 8.6%, respectively; p=0.0035, OR=4.90, 95% CI: 1.26- 18.51). Moreover, renal sequelae were more common in patients carrying the mutant T allele (p=0.0076, OR=2.20, 95% CI: 1.17-4.14)., Conclusions: Our results support that the IL1ß rs16944 polymorphism may be a potential marker of severe renal manifestations and renal sequelae in HSP.

Published
2016

13. HLA-DRB1 association with Henoch-Schonlein purpura.

Author

López-Mejías R, Genre F, Pérez BS, Castañeda S, Ortego-Centeno N, Llorca J, Ubilla B, Remuzgo-Martínez S, Mijares V, Pina T, Calvo-Río V, Márquez A, Sala-Icardo L, Miranda-Filloy JA, Conde-Jaldón M, Ortiz-Fernández L, Rubio E, León Luque M, Blanco-Madrigal JM, Galíndez-Aguirregoikoa E, González-Vela MC, Ocejo-Vinyals JG, González Escribano F, Martín J, Blanco R, and González-Gay MA

Abstract

Objective: Henoch-Schönlein purpura (HSP) is the most common vasculitis in children but it is not exceptional in adults. Increased familial occurrence supports a genetic predisposition for HSP. In this context, an association with the human leukocyte antigen-HLA-DRB1*01 phenotype has been suggested in Caucasian individuals with HSP. However, data on the potential association of HSP with HLA-DRB1*01 were based on small case series. To further investigate this issue, we performed HLA-DRB1 genotyping of the largest series of HSP patients ever assessed for genetic studies in Caucasians. Methods: 342 Spanish patients diagnosed with HSP fulfilling the American College of Rheumatology and the Michel et al classification criteria, and 303 sex and ethnically matched controls were assessed. HLA-DRB1 alleles were determined using a PCR-Sequence-Specific-Oligonucleotide Probe (PCR-SSOP) method. Results: A statistically significant increase of HLA-DRB1*01 in HSP patients when compared with controls was found (43% vs 7%, respectively; p<0.001; odds ratio-OR=2.03 [1.43-2.87]). It was due to the increased frequency of HLA-DRB1*0103 phenotype in HSP (14% vs 2%; p<0.001; OR=8.27 [3.46-23.9]). These results remained statistically significant after adjusting for Bonferroni correction. In contrast, a statistically significant decreased frequency of the HLA-DRB1*0301 phenotype was observed in patients compared to controls (5.6% vs 18.1%, respectively; p<0.001, OR=0.26 [0.14-0.47]), even after adjustment for Bonferroni correction. No HLA-DRB1 association with specific features of the disease was found. Conclusion: Our study confirms an association of HSP with HLA-DRB1*01 in Caucasians. Also, a protective effect against the development of HSP appears to exist in Caucasians carrying the HLA-DRB1*03 phenotype. This article is protected by copyright. All rights reserved., (Copyright © 2014 American College of Rheumatology.)

Published
2015
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