Abstract Germinal center (GC) formation in P. chabaudi rodent malaria is delayed for three weeks, which can prolong the infection. T follicular helper (Tfh) cells express CXCR5 for homing to the B cell area, and IL-21 which promotes antibody production. T helper type 1 (Th1) cells express CXCR3 and IFN-γ to promote phagocytosis. Previous data suggests that Th1 responses control peak parasitemia while systemic Th1 cytokines inhibit GC formation. In P. chabaudi, majority of CD4+ effector T cells (Teff) express markers of both Th1 and Tfh (e.g., CXCR5, CXCR3, Th1/Tfh hybrid), including IFN-γ and IL-21. The contribution of Th1/Tfh hybrid T cells in protection and antibody production remains unclear. We tested the impact of Il21+Tfh-like, Ifng+Th1-like, and Ifng+Il21+Th1/Tfh in protection by transferring these subsets from infected triple cytokine reporters (Il21-rfp Il4-gfp Ifng-Thy1.1) into TCR KO mice that are then infected. We are currently assessing changes in parasitemia and pathology. We found that Th1/Tfh cells do not help in vivo like recent data suggest they do in vitro. Th1/Tfh significantly generated few GC B cells, compared to Il21+ Tfh-like cells. Recipients of Th1-like cells had significantly lower parasite-specific IgG and GCs by immunohistology than Tfh-like at 21 dpi, hybrid Th1/Tfh were intermediate. A cytokine kinetics study of Th subsets in infected cytokine reporter mouse distinguished Il4+Il21+ GC Tfh from Th1 cells. The inflammation-driven chemokine receptors CXCR3 and CXCR6 are highly expressed on GC Tfh and Th1/Tfh hybrid during the first week of infection, but decline as GCs develop, suggesting a role for T cell migration which could explain the delay in GC formation and parasite-specific antibody production in malaria. Supported by R01AI 135061