TCR beta Combinatorial Immunoreceptor Expression by Neutrophils Correlates with Parasite Burden and Enhanced Phagocytosis during a Plasmodium berghei ANKA Malaria Infection

Recent studies have demonstrated that a subpopulation of neutrophils express the TCR alpha beta combinatorial immunoreceptor in humans and mice. Here, we report that a Plasmodium berghei ANKA murine malaria infection induces expansion of TCR beta expressing CD11b(+) Ly6G(+) neutrophils in the spleen during the early phase of infection. Measurement of TCR beta transcript and protein levels of neutrophils in wildtype versus nude and Rag1 knockout mice establishes that the observed expression is not a consequence of nonspecific antibody staining or passive receptor expression due to phagocytosis or trogocytosis of peripheral T cells. Remarkably, on day 3 postinfection, we observed a highly significant correlation between the proportion of neutrophils that express TCR beta and peripheral blood parasite burden. In addition, TCR beta(+) neutrophils phagocytose parasitized erythrocytes with 4-fold greater efficiency than TCR beta(-) neutrophils. Together these results signify that TCR expression by the neutrophil plays an important role in the regulation of parasite burden by enhancing the phagocytic capacity of the neutrophil.