Genetically engineered mice with a targeted disruption in the beta 2-microglobulin (beta 2-m) gene or the H2-I-A beta chain (A beta) which lack functional CD8+ or CD4+ T cells, respectively, were used to assess the role of T cell subsets in Brucella abortus infection. Murine brucellosis was markedly exacerbated in beta 2-m-deficient mice (beta 2-m-/-) compared to A beta mutant (A beta-/-) or C57BL/6 mice, strongly indicating that optimal resistance to B. abortus requires CD8+ T cells. Splenocytes from Brucella-primed beta 2-m-/-, A beta-/- and C57BL/6 mice exhibited a type 1 cytokine profile marked by elevated IFN-gamma mRNA expression and protein production, and basal levels of IL-2 and IL-4 transcripts. B. abortus did not induce secretion of TGF-beta 1, but substantial IL-10 activity was detected in spleen cell supernatants from all mouse strains studied. CD8+ T cells from A beta-/- and C57BL/6 mice displayed a CD44hi CD45RBlo phenotype and a type 1 cytokine transcription profile featuring high levels of IFN-gamma mRNA. Additionally, we have shown the ability of C57BL/6 CD8+ CTL to kill Brucella-infected macrophages. This study illustrates the predominant role of MHC class I-restricted T cells in controlling B. abortus infection.
Mendeley saves you time finding and organizing research
Choose a citation style from the tabs below