Activation of antigen receptor genes rearrangement in peripheral blood T lymphocytes as a possible mechanism of autoimmunity induction.

摘要

Under normal conditions, the main population of T cells, namely αβT cells differentiate in the thymus, where antigen receptor development and clonal selec tion processes providing deletion of autospecific T lymphocytes occur. Nevertheless, according to recent literature data, under certain physiological and patho logical conditions, repeated rearrangements of anti gen receptor (T cell receptor, TCR) genes seems to be induced in mature peripheral T lymphocytes. As a result, a new receptor with modified specificity appears on the membrane surface [1, 2]. Since there are no factors for effective clonal selection of such T lymphocytes in lymphoid organs, their development would inevitably create a threat of autoimmune dis eases. It is natural that the phenomenon of TCR gene rearrangement at the periphery was first demon strated, is stably detected and, hence, can be studied in mice prone to spontaneous autoimmune diseases, such as type I diabetes mellitus (nonobese diabetic (NOD) mice) and lupuslike syndrome (NZB × NZW hybrids) [3, 4].