Медицинская иммунология (Jul 2025)
Tumorigenesis as an autoimmune process
Abstract
The data presented in the article reasonably indicate that the immune system responses during the development of autoimmune pathology and in the process of tumor growth are, in fact, autoimmune responses directed at autoantigens of various tissues and organs, and tumor-associated antigens. The latter, in addition to the tumor itself, are also expressed by the cells of normal organs and tissues. At the same time, the differences are characterized by insufficient activity of suppressor cells in the first variant, and enhanced activity in the second variant. One should take into account a potential identity of the mechanisms of lymphocyte responses, both in autoimmune pathology and in oncogenesis. The concept of autoimmunity promoting the tumor development is a fundamentally important point, with regard of the tumor growth biology. In view of medicine, this approach may provide a vector for searching novel drug effects aimed at inhibiting the suppressor activity of regulatory cells, without higher risk of inducing autoimmune disorders. On the basis of available literature data, one may suggest that the formation of autoimmune pathology is caused by the impaired mechanisms of immune tolerance to autoantigens. Moreover, these mechanisms concern both central tolerance and peripheral tolerance. In the first case, T cells bearing high-affinity receptors directed against autoantigens are not subject to negative selection in the thymus and migrate to the periphery, being ready to induce autoimmune processes. At the same time, peripheral T regulatory suppressor cells do not work with respect to suppression of their activity. There is an evident disturbance of the both central and peripheral tolerance mechanisms. In the case of tumor growth, it has been shown that suppression of T regulatory cells results in development of autoimmune pathology, along with inhibition of tumor growth. The recent data from the literature allow us to suggest a targeted reaction of immune cells against tumor-associated antigens, and not against tumor-specific antigens. One should assume that these T cell effectors against tumor-associated antigens also have reached the peripheral tissues after migration from the thymus, without undergoing negative selection. However, their antitumor activity on the periphery could be suppressed by T regulatory cells. Apparently, it should be considered that the immune response to tumor growth exhibited features of an autoimmune response to tumor-associated antigens with induction of its activities by means of T regulatory immune cells.
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