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The ligand for CD40 (CD40L) is expressed on the surface of activated CD4+ T cells and its role in T-B cell collaborations and thymus-dependent humoral immunity is well established. Recently, by generating CD40L-knockout mice, we have confirmed its previously described role in humoral immunity and defined another important function of this molecule in the in vivo clonal expansion of antigen-specific CD4+ T cells. Here, we investigated the potential in vivo role of CD40L in antiviral immunity by examining the immune response mounted by CD40L-deficient mice following infection with lymphocytic choriomeningitis virus (LCMV), Pichinde virus, or vesicular stomatitis virus. Humoral immune responses of CD40L-deficient mice to these viruses were severely compromised, although moderate titres of antiviral IgM and some IgG2a were produced by virus-infected CD40L-deficient mice by a CD4+ T cell-independent mechanism. By contrast, CD40L-deficient mice made strong primary CTL responses to all three viruses. Interestingly however, although memory CTL activity was detectable in CD40L-deficient mice two months after infection with LCMV, the memory CTL response was much less efficient than in wild-type mice. Together, the results show that CD40-CD40L interactions are required for strong antiviral humoral immune responses, and reveal a novel role for CD40L in the establishment and/or maintenance of CD8+ CTL memory.

Type

Journal article

Journal

J Exp Med

Publication Date

01/05/1996

Volume

183

Pages

2129 - 2142

Keywords

Animals, Antibodies, Viral, Antibody Formation, B-Lymphocytes, CD4-Positive T-Lymphocytes, CD40 Antigens, CD40 Ligand, Immunoglobulin G, Immunoglobulin M, Immunologic Memory, Immunotherapy, Adoptive, Membrane Glycoproteins, Mice, Mice, Knockout, Reference Values, Rhabdoviridae Infections, Spleen, T-Lymphocytes, Cytotoxic, Thymus Gland, Vesicular stomatitis Indiana virus