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№4' 2016


International Medical Journal, Vol. 22., Iss. 4, 2016, P. 77−82.


Serbina I. M.

Kharkiv Medical Academy of Postgraduate Education, Ukraine

Alopecia areata (AA) is currently considered a tissue−specific autoimmune disease, which is mediated by autoactivated T−lymphocytes in conditions of immune tolerance (IT) impairment of the hair follicles and presentation of their own autoantigens. Melanocyte− and/or antigen−associated autoantigen of hair follicles (keratin 44/46 kDa and trichohyaline) are considered autoantigens in the majority of cases. Genetic predisposition and trigger factors lead to deactivation of immunosuppresive cytokines and factors of growth, which stimulate peripheral tolerance. Degranulation of mast cells and intensified production of TNF−? occur in the foci of AA. Active synthesis of IFN−? is observed, which stimulates expression of class II MHC molecules by follicular epithelium, which results in presentation of follicular autoantigens to CD8+ cells and loss of IT. IFN−? can also cause expression of class II MHC molecules by follicular epithelium, which leads to accumulation of CD4+ cells, which increase the activity of CD8+ cells due to synthesis of proinflammatory cytokines. During progressive stage of the disease a higher expression of adhesion molecules (ICAM−2 and ELAM−1) is recorded in perivascular and peribulbar zones of the involved area. Equally, the level of ligand Fas (a molecule which induces apoptosis of activated T−cells) is significantly decreased. Some genes associated with AA and other autoimmune diseases were identified. Increased emphasis is on ULBP3 (cytomegalovirus binding protein) (6q25), which codes activation of ligands of NK−cellular receptor NKG2D, which initiates autoimmune response.

Key words: alopecia areata, pathogenesis, immune disorders, immune privilege.

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