Expansion of the CD4−, CD8− γδ T cell subset in the spleens of mice during non-lethal blood-stage malaria

Splenic γδ T cells (CD4^?, CD8^?) increased more that 10-fold upon resolution of either Plasmodium chabaudi adami or P. c. chabaudi infections in C57BL/6 mice compared to controls. Similarly, a 10- to 20-fold expansion of the γδ T cell population was observed in β₂-microglobulin deficient (β²-m^0.0) mice that had resolved P. c. adami, P. c. chabaudi or P. yoelii yoelii infections. In contrast, increases in the number of splenic αβ T cells in these infected mice were only two to three-fold indicating a differential expansion of the γδ T cell subset during malaria. Because nucleated cells of β₂-m^0/0 mice lack surface expression of major histocompatibility complex class I and class Ib glycoproteins, our findings suggest that antigen presentation by these glycoproteins is not necessary for the increasing number of γδ T cells. Our observation that after resolution of P. c. adami malaria, C57BL/6 mice depleted of CD8⁺ cells by monoclonal antibody treatment had lower numbers of γδ T. cells than untreated controls suggests that the demonstrated lack of CD8⁺ cells in β₂-m^0/0 mice does not contribute to the expansion of the γδ T cell population during non-lethal malaria.