T cell subsets in granulomatous inflammation and immunity to L. Monocytogenes and B. abortus.

The phenomenological reevaluation of cellular immunity to L. monocytogenes and B. abortus revealed that the inflammatory reactions accompanying both infections, i.e. DTH, splenomegaly and granulomatous inflammation, are mediated exclusively by CD4+ T cells. On the other hand, as shown in the acute Listeria-model as well as in the more chronic murine Brucellosis, specific CD8+ T cells are able to mediate protective mechanisms in the absence of any granulomatous monocyte accumulation. In an attempt to determine the cytokines responsible for monocyte accumulation and antibacterial protection we could show that IFN-gamma and TNF, both discussed as proinflammatory as well as macrophage activating cytokines, both can be produced in a T-cell-dependent as well as in a T-cell-independent manner. The ability of listeria-specific CD8+T cells to secrete TNF and IFN-gamma in response to listerial antigen argues against a role of these cytokines as mediators of granuloma formation.