A New Link between γδ T Cells and Myeloid Cells in Malaria? Matthew D. Lewis, Jean Langhorne  Immunity  Volume 48, Issue 2, Pages 193-195 (February 2018) DOI: 10.1016/j.immuni.2018.02.003 Copyright © 2018 Elsevier Inc. Terms and Conditions

Figure 1 A Model Detailing Early and Late Immune Responses Leading to Control of Chronic Malaria Infection via M-CSF Produced by γδ T Cells Based on the findings of Mamedov et al. and previous studies, we propose that during early malaria infection, αβ T cells become activated, expanding to their highest frequency at peak parasitemia, and produce M-CSF, promoting the expansion and activation of the myeloid compartment; γδT-IFN-γ cells produce IFN-γ (1). Macrophages control infection by the phagocytic clearance of infected red blood cells (2). Over time, B cells are activated and differentiate into antibody-secreting cells (3). Later, at the chronic stage of infection, γδT-M-CSF cells activate, expand in the spleen, and produce M-CSF (4). This and other environmental factors might promote epigenetic reprogramming of the macrophage into a “trained” state (5). Free immunoglobulins produced by antibody-secreting cells opsonize free merozoites or infected red blood cells (6). “Trained” macrophages control infection by phagocytosis of infected red blood cells or free merozoites, either with (7), or without (8) the recognition of opsonizing antibody. Immunity 2018 48, 193-195DOI: (10.1016/j.immuni.2018.02.003) Copyright © 2018 Elsevier Inc. Terms and Conditions