These observations, together with our findings that B cell-deficient mice with chronic TB exhibit diminished lung inflammation that is associated enhanced pulmonic IL-10 expression; and that IL-10 signaling blockade can reverse the inflammation and CD4+ T cell phenotypes, suggests that B cells play a role in restricting the expression of the immunosuppressive and anti-inflammatory IL-10 so as to optimize the expression of IFN-γ-producing CD4+ T, perhaps at the expense of the risk of the development of host tissue-damaging immunopathology. The gene discussed is IFNG; the disease is tuberculosis.