Formation of autoimmune effectors after transfer of virus-induced autoreactive precursors to syngeneic intact receptor animals.
We verified the assumption that autoimmune responses underlie immunosuppression developing in the course of virus infection. It has been shown by adoptive transfer that administration of Langat-virus-induced autoreactive lymphocytes (ARL) to the syngeneic recipient is followed by accumulation of autoreactive effectors (AE) eliciting a graft-verus-host reaction (GVHR) in the syngeneic system (AEgvhr). In addition, cytotoxic T-lymphocytes (AEc) appeared against the syngeneic macrophages. This effect was mediated by the H-2 restriction principle for ARL donors and their recipients. The infection triggered a T-suppressor-mediated reaction inhibiting the differentiation of precursors into mature autoreactive effectors. In the absence of T-cell suppressor effect (on consecutive syngeneic transfer) ARL will cause systemic pathologic changes in the recipients, namely, infiltrative and necrotic lesions in different organs and tissues. This mechanism is attributed to the activation of precursors in the body of intact recipient and to the formation of mature effectors owing to cytokines released by donor ARL.
D000818:Animals; D001323:Autoantibodies / Q000096:biosynthesis*; D004669:Encephalitis Viruses, Tick-Borne / Q000276:immunology*; D005416:Flavivirus / Q000276:immunology*; D006087:Graft vs Host Reaction; D006183:H-2 Antigens / Q000276:immunology; D007108:Immune Tolerance; D007116:Immunization, Passive; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D013154:Spleen / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D001323:Autoantibodies; D006183:H-2 Antigens