Seminar In Medicine, 27.04.2018, Sešil Vural, M.D.

Author: KUSOM
Time: 15:00
Location: MED 176



Friday, April 27th, 2018

Speaker          : Dr. Seçil Vural, Ludwig-Maximillians University / Research Laboratory

 Tittle             : MHC-I-opathy and Autoinflammation from Dermatological Perspective

Time              : 15.00 (Refreshments will be served at 14:45)

Place              : MED 176

TelePresence   : AH 5th floor Chief Medical Officer / KUH 9th floor Meeting Room


MHC-I-opathy and Autoinflammation from Dermatological Perspective

HLA class I alleles are present in virtually all the cells. They present antigens derived from cytoplasmic proteins to CD8 T cells. Genetic variation in HLA-I genes in the Major Histocompatibility locus have a strong disease linkage in three diseases: HLA-B*27 with ankylosing spondylitis, HLA-B*51 with Behçet’s disease and HLA-C*0602 with psoriasis. HLA-I connection in these diseases designate CD8 T cells as the key-player in the pathogenesis.

In psoriasis, CD8 T cells dominating the lesion preferentially use Vβ3 and Vβ13S1 T-cell receptor (psoriatic TCR). Recently a Vα3S1/Vβ13S1 T-cell receptor (TCR) was reconstituted from an epidermal CD8+ T-cell clone of an HLA-C*06:02–positive psoriasis patient. By using the conserved amino-acid pattern for psoriatic TCR we selected peptides from food and pathogens as candidate environmental antigens that may initiate the psoriatic autoimmune response. Several environmental antigens triggered the melanocyte-specific autoimmune response in psoriasis in experimental settings.  In another MHC-I-opathy, Behçet’s disease CD8+ T cells are increased in lesional skin. We identified the major infiltrating the lesion as CD8 T cells secreting interleukin 17 by immunohistochemistry. These findings suggest a similar pathogenesis in both MHC-I-opathies.

By identifying and avoiding etiological triggers for MHC-I-opathies we may develop strategies to prevent disease onset and exacerbation.