Regulation of macrophage Ia expression in mice with severe combined immunodeficiency: induction of Ia expression by a T cell-independent mechanism.
We have studied the expression of Ia molecules by macrophages from mice with severe combined immunodeficiency (CB-17 scid) that lack demonstrable T cell and B cell functions. CB-17 scid mice had approximately normal numbers of Ia-bearing macrophages in the peritoneal cavity, spleen, and liver. Peritoneal macrophages responded in culture to T cell-derived lymphokines with enhanced expression of Ia molecules. However, unlike immunocompetent controls, SCID mice could not enhance Ia expression in an antigen-specific T cell-dependent manner after secondary challenge in vivo with a conventional protein antigen such as hemocyanin. Further demonstration of their T cell deficiency was the failure of CB-17 scid spleen cells to proliferate and produce IL 2 in response to the T cell mitogen, concanavalin A. Upon infection with Listeria monocytogenes, CB-17 scid mice developed chronically high loads of bacteria, whereas CB-17 control mice eliminated all viable bacteria and became resistant to secondary infection. However, Listeria-infected CB-17 scid mice did show, in parallel with the CB-17 controls, an unexpected and striking increase of Ia-positive macrophages. These data indicate that induction of Ia expression in macrophages can occur via a mechanism that is independent of mature T cells.
D000818:Animals; D000955:Antigens, T-Independent / Q000276:immunology*; D006433:Hemocyanins / Q000494:pharmacology; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis*; D007153:Immunologic Deficiency Syndromes / Q000276:immunology*; D008089:Listeria monocytogenes / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D008815:Mice, Inbred Strains; D008817:Mice, Mutant Strains; D010529:Peritoneal Cavity; D013601:T-Lymphocytes / Q000276:immunology*
D000955:Antigens, T-Independent; D000949:Histocompatibility Antigens Class II; D006433:Hemocyanins