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H-2 restricted regulation by soluble autoantigens of the tick-borne encephalitis virus-induced autoreactive T-effector and T-suppressor lymphocytes in mice.

Soluble autoantigens (mouse red blood cells lysed by sonication) blocked in vitro the antigen-recognizing receptors of tick-borne encephalitis (TBE) virus-induced autoreactive T-lymphocytes (ARTL), effectors of the local graft-versus-host reaction (GVHR) in a syngeneic system and prevented the development of GVHR in vivo. Antigen-recognizing receptors were also found on T-suppressors (Ts) that became activated during experimental tick-borne encephalitis in mice and inhibited the activity of ARTL. The interaction between these receptors and autoantigens in vitro resulted in a loss of the ability of Ts to inhibit in vivo the ARTL-mediated GVHR. A similar result was obtained with ARTL and Ts activated in mice infected with Langat, dengue type 2 (D2) and yellow fever (strain 17D) viruses. The block of the antigen-recognizing receptors of T-cells was reversible, and not associated with lymphokine production or effector death. The block of the antigen-recognizing receptors in vitro and the loss of the corresponding T-cell function in vivo occurred provided that the donors of soluble erythrocyte antigens (SEA) and of the lymphocytes had at least one common major histocompatibility complex (MHC) haplotype. Injection SEA from donors whose H-2 complex haplotypes were identical to those of TBE-infected recipients prevented in the latter the formation of ARTL or Ts. The autoantigens inhibiting the ARTL and Ts activities seemed to be products of the MHC genes. The role of soluble H-2 autoantigens in preventing virus-induced autoimmune reaction and maintaining a state of natural immunological tolerance is discussed.