Il-4 is an endogenous T cell growth factor during the immune response to a syngeneic retrovirus-induced tumor

J Immunol. 1988 Oct 15;141(8):2824-30.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antibodies / pharmacology
  • Antigens, Differentiation, T-Lymphocyte
  • Cell Transformation, Viral / drug effects
  • Epitopes / immunology
  • Female
  • Friend murine leukemia virus
  • Immunosuppressive Agents / pharmacology
  • Interleukin-2 / biosynthesis
  • Interleukin-2 / immunology
  • Interleukin-2 / physiology*
  • Interleukin-4
  • Interleukins / biosynthesis
  • Interleukins / physiology*
  • Leukemia, Erythroblastic, Acute / genetics
  • Leukemia, Erythroblastic, Acute / immunology*
  • Leukemia, Erythroblastic, Acute / pathology
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Inbred CBA
  • Spleen / immunology
  • T-Lymphocytes, Cytotoxic / classification
  • T-Lymphocytes, Cytotoxic / immunology

Substances

  • Antibodies
  • Antigens, Differentiation, T-Lymphocyte
  • Epitopes
  • Immunosuppressive Agents
  • Interleukin-2
  • Interleukins
  • Interleukin-4