Alopecia areata (AA) is regarded as a tissue-specific autoimmune disease of hair follicles.
CD8+ T cells are considered to act as the effector cells with help from CD4+ T cells
[
[1]
]. Various autoantibodies have also been found in the sera [
2
,
3
]. These antibodies may not play a primary direct role in AA pathogenesis; however,
the production of these antibodies suggests that B cells are excessively activated
in AA.To read this article in full you will need to make a payment
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References
- Alopecia areata: autoimmune basis of hair loss.Eur J Dermatol. 2004; 14: 364-370
- Serum anti-Fcgamma receptor autoantibodies in patients with alopecia areata.Arch Dermatol Res. 2006; 298: 493-498
- Hair follicle structures targeted by antibodies in patients with alopecia areata.Arch Dermatol. 1997; 133: 57-61
- BLyS: member of the tumor necrosis factor family and B lymphocyte stimulator.Science. 1999; 285: 260-263
- BAFF AND APRIL: a tutorial on B cell survival.Annu Rev Immunol. 2003; 21: 231-264
- Impact of the BAFF/BR3 axis on B cell survival, germinal center maintenance and antibody production.Semin Immunol. 2006; 18: 290-296
- The role of the BAFF/APRIL system on T cell function.Semin Immunol. 2006; 18: 284-289
- Epithelial cells trigger frontline immunoglobulin class switching through a pathway regulated by the inhibitor SLPI.Nat Immunol. 2007; 8: 294-303
- Serum levels of BAFF are increased in bullous pemphigoid but not in pemphigus vulgaris.Br J Dermatol. 2006; 155: 330-336
- Increased serum levels of a proliferation-inducing ligand in patients with bullous pemphigoid.J Dermatol Sci. 2007; 46: 53-60
Article info
Publication history
Published online: July 12, 2010
Received:
August 2,
2007
Identification
Copyright
© 2008 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
