Role of T cell subsets in immunity against intracellular bacteria: experimental infections of knock-out mice with Listeria monocytogenes and Mycobacterium bovis BCG.

The generation of knock-out mice with targeted gene deletions has already proven its enormous value for our understanding of the antimicrobial immune response. Here, we describe studies with knock-out mice deficient in the TCR-beta gene, lacking alpha/beta T cells; in the TCR-delta gene, lacking gamma/delta T cells; in the beta 2m gene, lacking beta 2-microglobulin, and hence cell surface expressed MHC class I and functional CD8 T cells; and in the H-2I-A beta gene, lacking cell surface expressed MHC class II and hence functional CD4 T cells. These mice were infected with Listeria monocytogenes or Mycobacterium bovis BCG as representative microbes which primarily activate CD8 T cells or CD4 T cells, respectively. Data described in this treatise demonstrate that the different gene deletions had an impact of varying degree on antibacterial defense and on the formation of granulomatous lesions. At the same time, the data point to a compensatory potential of the incomplete immune system. We assume that deletions in the major immune effector cells promote the emergence of a second line of defenders which frequently remain silent in the normal immune system. Thus, our data illustrate an enormous redundancy of the immune system, which, however, is not abundant since it takes over essential functions in the immunodeficient situation.