CD36 regulates malaria-induced immune responses primarily at early blood stage infection contributing to parasitemia control and resistance to mortality [Immunology]

In malaria, CD36 plays several roles including mediating parasite sequestration to host organs, phagocytic clearance of parasites and regulation of immunity. While the functions of CD36 in parasite sequestration and phagocytosis have been clearly defined, less is known about its role in malaria immunity. Here, to understand the function of CD36 in malaria immunity, we studied parasite growth, innate and adaptive immune responses, and host survival in WT and Cd36-/- mice infected with a nonlethal strain of Plasmodium yoelii. Compared to Cd36-/- mice, WT mice had lower parasitemias and were resistant to death. At early but not at later stages of infection, WT mice had higher circulatory pro-inflammatory cytokines and lower anti-inflammatory cytokines than Cd36-/- mice. WT mice showed higher frequencies of pro-inflammatory cytokine-producing and lower frequencies of anti-inflammatory cytokine-producing DCs and NK cells than Cd36-/- mice. Cytokines produced by co-cultures of DCs from infected mice and OT-II T cells reflected CD36-dependent DC function. WT mice also showed increased Th1 and reduced Th2 responses than Cd36-/- mice, mainly at early stages of infection. Furthermore, in infected WT mice, macrophages and neutrophils expressed higher levels of phagocytic receptors and showed enhanced phagocytosis of parasite-infected erythrocytes than those in Cd36-/- mice, in an IFN-γ-dependent manner. However, there were no differences in malaria-induced humoral responses between WT and Cd36-/- mice. Overall, the results show that CD36 plays a significant role in controlling parasite burden by contributing to pro-inflammatory cytokine responses by DCs and NK cells, Th1 development, phagocytic receptor expression, and phagocytic activity.

from #AlexandrosSfakianakis via Alexandros G.Sfakianakis on Inoreader http://ift.tt/2oiQnxa
via IFTTT