Il-4 is an endogenous T cell growth factor during the immune response to a syngeneic retrovirus-induced tumor.
The relative contributions of IL-2 and IL-4 during the immune response to the retrovirus-induced tumor, FBL, were examined. Both proliferative and cytolytic responses to FBL were measured and compared to similar responses to minor histocompatibility Ag. The addition of alpha IL-2 partially inhibited FBL-stimulated proliferation of purified L3T4+ T cells and nearly completely inhibited the response of Lyt-2+ T cells, whereas alpha IL-4 partially inhibited the proliferative response of the L3T4+ subset but had no effect on the response of the Lyt-2+ subset. The addition of exogenous IL-4 augmented the proliferative response of both subsets. Therefore, IL-4 is an endogenous growth factor for FBL-induced specific proliferation of the L3T4+ and not the Lyt-2+ population, but both subpopulations can respond to IL-4. Similar examination of anti-FBL CTL responses revealed that alpha IL-2, but not alpha IL-4, inhibited FBL-specific Lyt-2+ CTL generation. However, exogenous IL-4 partially replaced the L3T4+ Th cell activity necessary for optimal Lyt-2+ FBL-specific CTL generation. Therefore, IL-4 is not required but can participate in the CTL response. The role of IL-4 during the immune response of B6 mice to minor histocompatibility Ag disparate BALB.B cells was analyzed. alpha IL-4 had no detectable effect on the proliferative or cytolytic response to BALB.B cells, suggesting that endogenous IL-4 does not have a significant role in these responses. The extent of involvement of endogenous IL-4 in the T cell responses to retrovirus-induced tumor Ag and minor histocompatibility Ag presumably reflects the nature of the stimulating Ag, and detection of an IL-4 response may correlate with induction of an antibody response. Thus, the immunizing Ag and/or host B cell repetoire may influence which subsets of L3T4+ Th cells are activated during priming in vivo.
Kern
D E
DE
Department of Microbiology/Immunology, University of Washington, Seattle 98195.
Peace
D J
DJ
Klarnet
J P
JP
Cheever
M A
MA
Greenberg
P D
PD
D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D000945:Antigens, Differentiation, T-Lymphocyte; D002472:Cell Transformation, Viral / Q000187:drug effects; D000939:Epitopes / Q000276:immunology; D005260:Female; D005622:Friend murine leukemia virus; D007166:Immunosuppressive Agents / Q000494:pharmacology; D007376:Interleukin-2 / Q000096:biosynthesis / Q000276:immunology / Q000502:physiology*; D015847:Interleukin-4; D007378:Interleukins / Q000096:biosynthesis / Q000502:physiology*; D004915:Leukemia, Erythroblastic, Acute / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D008213:Lymphocyte Activation; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D013154:Spleen / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000145:classification / Q000276:immunology
D000906:Antibodies; D000945:Antigens, Differentiation, T-Lymphocyte; D000939:Epitopes; D007166:Immunosuppressive Agents; D007376:Interleukin-2; D007378:Interleukins; D015847:Interleukin-4