Virus-induced decrease in the activity of serum blocking factor(s): a mechanism of activation of the autoreactive T effectors in graft versus host reaction and of controlling T suppressors.

It has been shown that serum blocking factor(s) (SBF) previously detected in normal mice bind(s) to receptors on the surface membranes of virus-induced autoreactive T lymphocytes (ARTL) and to that of ARTL activity inhibiting T suppressors (TSar). The interaction of SBF with the receptors is reversible, H-2 restricted and associated with the inhibition of functional activity of the tested T lymphocyte populations. In mice during acute tick-borne encephalitis (TBE), in the course of inapparent infections induced by Langat virus or dengue type 2 (D2) and after infection with the attenuated yellow fever virus (strain 17D), the SBF activity significantly decreased, while ARTL and TSar became activated. Administration of normal mouse serum to infected animals with SBF deficiency resulted in inhibition of both inductive and productive phases of ARTL and TSar formations. Based on these findings, the virus-induced decrease in SBF activity may be considered as one of the mechanisms triggering autoimmune responses. The autoreactive pathological states can develop under various endo-and/or exogenic conditions influencing on SBF and on the TSar activity.