The importance of an IFNγ CD4+ T cell response in mediating protection from anthrax infection in vivo [48], in addition to the increased survival and B. anthracis bactericidal activity of IFNγ activated macrophages [128], and the disproportionate focus of LT upon suppressing IFNγ release by NK cells [129], suggests that survival of B. anthracis within the host depends in part, upon the suppression of a Th1 associated IFNγ release. Here, CD4 is linked to anthrax infection.