Dual role of B cells in mediating innate and acquired immunity to herpes simplex virus infections

Abstract

mu-immunoglobulin chain gene targeted B-cell-deficient mice of susceptible BALB/c strain and resistant C57B1/6 strain are up to 100- to 1000-fold more susceptible to cutaneous infection by herpes simplex virus (HSV) than the respective control wild type mice. The effect of the lack of B cells on immunity to HSV infections was analyzed and B cells were found to play a dual role in affecting both innate and acquired immune responses. Natural antibodies (IgM isotype), reactive with HSV have an anti-viral effect in the innate control of primary cutaneous HSV infection. B cells can also function as antigen-presenting cells for the stimulation of HSV-specific CD4+ T-cell responses. Consequently, CD4+ T cells and interferon-gamma responses were found to be significantly impaired in HSV-infected B-cell-deficient mice compared to that seen in control mice. No significant differences were found in natural-killer-cell- or HSV-specific CD8+ T-cell activity between control and B-cell-deficient mice. Our results imply a role for B cell in mediating innate and CD4+ T-cell-specific immunity in determining susceptibility to primary HSV infections.