CD36 regulates malaria-induced innate immune responses

• Published in: The Journal of immunology (1950) 2017-05, Vol.198 (1_Supplement), p.68-68.11
• Main Authors: Puttalingaiah, Ramesh Thylur, Wu, Xianzhu, Gowda, Nagaraj M, Punnath, Kishore, Gowda, Channe D
• Format: Article
• Language: English
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.198.Supp.68.11

Malaria causes enormous morbidity and mortality worldwide. However, an effective vaccine is not yet available due to the knowledge gap in various molecular and cellular processes involved in protective immunity development. CD36, a multifunctional scavenger receptor, plays several important roles in malaria, including sequestration of parasites in host organs, parasitemia control, and protective immunity. Although the role of CD36 in the former two processes has been well understood, less is known about the function of CD36 in the latter. We studied the role of CD36 in host survival and immune responses in non-lethal Plasmodium yoelii infected WT and CD36−/− mice. WT mice showed lower parasitemia and higher survival rate compared to the CD36−/− mice. At early but not at later stages of infection, the circulatory pro-inflammatory cytokines were higher and anti-inflammatory cytokines were lower in WT mice than in CD36−/− mice. DCs, NK and T cells of WT mice had higher frequencies of pro-inflammatory and lower frequencies of anti-inflammatory cytokine-producing cells than CD36−/− mice. Additionally, Th1 response was decreased, whereas Th2 response was increased in CD36−/− mice. Compared to CD36−/− mice, macrophages and neutrophils of WT mice showed higher phagocytic activity and phagocytic receptors expression in an IFN-g dependent manner. However no difference in the malaria-induced humoral responses between WT and CD36−/− mice was observed. Our data demonstrated that CD36 plays an important role in parasitemia control and protective immunity by upregulating pro-inflammatory cytokine responses by DCs and NK cells, promoting Th1 response, and contributing to phagocytic receptor expression and phagocytic activity.