Characterization of γδ T Cell Effector/Memory Subsets Based on CD27 and CD45R Expression in Response to Infection.

Tuberculosis (TB) remains a leading cause of death from infectious diseases worldwide. is the causative agent of bovine TB and zoonotic TB infection. γδ T cells are known to participate in the immune control of mycobacterial infections. Data in human and nonhuman primates suggest that mycobacterial infection regulates memory/effector phenotype and adaptive immune functions of γδ T cells. To date, the impact of infection on bovine γδ T cells and their effector and memory differentiation remains unknown. In this study, we show that circulating γδ T cells from -infected cattle can be differentiated based on the expression of CD27, which is indicative of their capacity to respond to virulent infection: CD27 γδ T cells proliferated in response to Ag and, thus, may comprise the adaptive γδ T cell compartment in cattle. We further show that bovine -specific γδ T cells express surface markers characteristic of central memory T cells (CD45RCD27CD62L) and that -specific CD4 and γδ T cells both upregulate the expression of the tissue-homing receptors CXCR3 and CCR5 during infection. Our studies contribute significantly to our understanding of γδ T cell differentiation during TB infection and provide important insights into the link between phenotypic and functional subsets in the bovine. Accurate characterization of γδ T cell effector and memory-like responses induced during mycobacterial infection will contribute to improved strategies for harnessing the γδ T cell response in protection against TB for humans and animals.