HLA Class II Polymorphism Contributes to Specify Desmoglein Derived Peptides in Pemphigus Vulgaris and Pemphigus Foliaceus

2000 ◽  
Vol 15 (1) ◽  
pp. 67-73 ◽  
Author(s):  
Pascale Loiseau ◽  
Laurence Lecleach ◽  
Catherine Prost ◽  
Virginia Lepage ◽  
Marc Busson ◽  
...  
2021 ◽  
Author(s):  
The Bich Thanh Vuong ◽  
Duc Minh Do ◽  
Phuc Thinh Ong ◽  
Thai Van Thanh Le

Background: Pemphigus is a group of rare, life-threatening bullous autoimmune diseases that affect the skin and mucous membranes and are associated with high morbidity and morbidity. HLA class II genes, particularly HLA-DRB1 and HLA-DQB1, play roles in pemphigus. Objectives: To investigate the susceptibility of HLA class II DRB1 and DQB1 alleles in Vietnamese patients with pemphigus vulgaris (PV) or pemphigus foliaceus (PF). Methods: The study enrolled 31 participants (22 with PV, 9 with PF) with diagnoses confirmed by clinical manifestations, histopathology, and direct immunofluorescence from November 2019 to June 2020. The HLA polymorphisms were determined by Sanger sequencing. The HLA-DRB1 and HLA-DQB1 profiles of the 101 healthy individuals in the control group have been published previously. Results: The frequencies of HLA-DRB1*14, DRB1*13:07, DRB1*04:04, DRB1*03:02, DQB1*02:02, and DQB1*05:03 were significantly higher, whereas those of DRB1*09:01, DRB1*12:02, DQB1*03:03, DQB1*05:01, and DQB1*06:01 were significantly lower, in the PV group than in the controls. The frequencies of DRB1*14:54, DRB1*13:07, and HLA-DQB1*03:02 were significantly higher in the PF group than in the controls. Conclusions: Alleles HLA-DRB1*14:54, DRB1*14:04, DRB1*14:03, DRB1*14:01, DRB1*14:12, DRB1*13:07, DRB1*04:04, DRB1*03:02, DQB1*02:02, and DQB1*05:03 were associated with an increased risk of PV, whereas alleles DRB1*09:01, DRB1*12:02, DQB1*03:03, DQB1*05:01, and DQB1*06:01 might protect against PV. In PF, DRB1*14:54, DRB1*13:07, and HLADQB1* 03:02 are promising susceptibility alleles.


2016 ◽  
Vol 72 ◽  
pp. 19-24 ◽  
Author(s):  
Maria José Franco Brochado ◽  
Daniela Francisca Nascimento ◽  
Wagner Campos ◽  
Neifi Hassan Saloum Deghaide ◽  
Eduardo Antonio Donadi ◽  
...  

1989 ◽  
pp. 429-432
Author(s):  
Stephen J. Scharf ◽  
Adam Friedmann ◽  
Chaim Brautbar ◽  
Fanny Szafer ◽  
Lawrence Steinman ◽  
...  

2006 ◽  
Vol 177 (9) ◽  
pp. 6517-6526 ◽  
Author(s):  
Hugo Mouquet ◽  
Sandrine Farci ◽  
Pascal Joly ◽  
Bernard Maillère ◽  
Jonathan Leblond ◽  
...  

2010 ◽  
Vol 130 (1) ◽  
pp. 311-314 ◽  
Author(s):  
Monika Saha ◽  
Karen Harman ◽  
Neil J. Mortimer ◽  
Valentina Binda ◽  
Martin M. Black ◽  
...  

1998 ◽  
Vol 52 (1) ◽  
pp. 74-77 ◽  
Author(s):  
Y. Yamashina ◽  
S. Miyagawa ◽  
T. Kawatsu ◽  
T. Iida ◽  
I. Higashimine ◽  
...  

2002 ◽  
Vol 3 (4) ◽  
pp. 205-210 ◽  
Author(s):  
P Martel ◽  
D Gilbert ◽  
M Busson ◽  
P Loiseau ◽  
V Lepage ◽  
...  

2021 ◽  
Vol 11 ◽  
Author(s):  
Inga Koneczny ◽  
Vuslat Yilmaz ◽  
Konstantinos Lazaridis ◽  
John Tzartos ◽  
Tobias L. Lenz ◽  
...  

IgG4 autoimmune diseases (IgG4-AID) are an emerging group of autoimmune diseases that are caused by pathogenic autoantibodies of the IgG4 subclass. It has only recently been appreciated, that members of this group share relevant immunobiological and therapeutic aspects even though different antigens, tissues and organs are affected: glomerulonephritis (kidney), pemphigus vulgaris (skin), thrombotic thrombocytopenic purpura (hematologic system) muscle-specific kinase (MuSK) in myasthenia gravis (peripheral nervous system) and autoimmune encephalitis (central nervous system) to give some examples. In all these diseases, patients’ IgG4 subclass autoantibodies block protein-protein interactions instead of causing complement mediated tissue injury, patients respond favorably to rituximab and share a genetic predisposition: at least five HLA class II genes have been reported in individual studies to be associated with several different IgG4-AID. This suggests a role for the HLA class II region and specifically the DRβ1 chain for aberrant priming of autoreactive T-cells toward a chronic immune response skewed toward the production of IgG4 subclass autoantibodies. The aim of this review is to provide an update on findings arguing for a common pathogenic mechanism in IgG4-AID in general and to provide hypotheses about the role of distinct HLA haplotypes, T-cells and cytokines in IgG4-AID.


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