scholarly journals Does autoimmune vitiligo protect against COVID‐19 disease?

2021 ◽  
Author(s):  
Nicoline F. Post ◽  
Rosalie M. Luiten ◽  
Albert Wolkerstorfer ◽  
Marcel Bekkenk ◽  
Markus Böhm
Keyword(s):  

1998 ◽  
Vol 188 (6) ◽  
pp. 1203-1208 ◽  
Author(s):  
Graham S. Ogg ◽  
P. Rod Dunbar ◽  
Pedro Romero ◽  
Ji-Li Chen ◽  
Vincenzo Cerundolo

Vitiligo is an autoimmune condition characterized by loss of epidermal melanocytes. Using tetrameric complexes of human histocompatibility leukocyte antigen (HLA) class I to identify antigen-specific T cells ex vivo, we observed high frequencies of circulating MelanA-specific, A*0201-restricted cytotoxic T lymphocytes (A2–MelanA tetramer+ CTLs) in seven of nine HLA-A*0201–positive individuals with vitiligo. Isolated A2–MelanA tetramer+ CTLs were able to lyse A*0201-matched melanoma cells in vitro and their frequency ex vivo correlated with extent of disease. In contrast, no A2–MelanA tetramer+ CTL could be identified ex vivo in all four A*0201-negative vitiligo patients or five of six A*0201-positive asymptomatic controls. Finally, we observed that the A2–MelanA tetramer+ CTLs isolated from vitiligo patients expressed high levels of the skin homing receptor, cutaneous lymphocyte-associated antigen, which was absent from the CTLs seen in the single A*0201-positive normal control. These data are consistent with a role of skin-homing autoreactive melanocyte-specific CTLs in causing the destruction of melanocytes seen in autoimmune vitiligo. Lack of homing receptors on the surface of autoreactive CTLs could be a mechanism to control peripheral tolerance in vivo.



2012 ◽  
Vol 22 (2) ◽  
pp. 279-280 ◽  
Author(s):  
Atsushi Tanemura ◽  
Tomoko Yajima ◽  
Mayuko Nakano ◽  
Megumi Nishioka ◽  
Saori Itoi ◽  
...  


2006 ◽  
Vol 16 (Supplement 1) ◽  
pp. S40
Author(s):  
P. Oyarbide-Valencia ◽  
J. van den Boorn ◽  
M. Li ◽  
C. Denman ◽  
J. Carlson ◽  
...  


2013 ◽  
Vol 22 (9) ◽  
pp. 566-569 ◽  
Author(s):  
Jeffrey A. Mosenson ◽  
Jonathan M. Eby ◽  
Claudia Hernandez ◽  
I. Caroline Le Poole


2018 ◽  
Vol 08 (03) ◽  
pp. 133-139
Author(s):  
Atsushi Tanemura ◽  
Lingli Yang ◽  
Ichiro Katayama
Keyword(s):  
T Cells ◽  


2014 ◽  
Vol 192 (4) ◽  
pp. 1433-1439 ◽  
Author(s):  
Katelyn T. Byrne ◽  
Peisheng Zhang ◽  
Shannon M. Steinberg ◽  
Mary Jo Turk


1995 ◽  
Vol 182 (5) ◽  
pp. 1609-1614 ◽  
Author(s):  
I Hara ◽  
Y Takechi ◽  
A N Houghton

The immune system can recognize differentiation antigens that are selectively expressed on malignant cells and their normal cell counterparts. However, it is uncertain whether immunity to differentiation antigens can effectively lead to tumor rejection. The mouse brown locus protein, gp75 or tyrosinase-related protein 1, is a melanocyte differentiation antigen expressed by melanomas and normal melanocytes. The gp75 antigen is recognized by autoantibodies and autoreactive T cells in persons with melanoma. To model autoimmunity against a melanocyte differentiation antigen, mouse antibodies against gp75 were passively transferred into tumor-bearing mice. Passive immunization with a mouse monoclonal antibody against gp75 induced protection and rejection of both subcutaneous tumors and lung metastases in syngeneic C57BL/6 mice, including established tumors. Passive immunity produced coat color alterations but only in regenerating hairs. This system provides a model for autoimmune vitiligo and shows that immune responses to melanocyte differentiation antigens can influence mouse coat color. Immune recognition of a melanocyte differentiation antigen can reject tumors, providing a basis for targeting tissue autoantigens expressed on cancer.



2016 ◽  
Vol 48 (11) ◽  
pp. 1418-1424 ◽  
Author(s):  
Ying Jin ◽  
Genevieve Andersen ◽  
Daniel Yorgov ◽  
Tracey M Ferrara ◽  
Songtao Ben ◽  
...  


1996 ◽  
Vol 75 (3) ◽  
pp. 351-356 ◽  
Author(s):  
G.F. ERF ◽  
J.R. SMYTH


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