Temporally evolving functions of IL-10 and IL-21 in regulating murine anti-plasmodium humoral immunity

Plasmodium parasites are the causative agent of the disease malaria, which, despite public health efforts, remains a global health burden with ~240 million clinical cases and ~620,000 deaths annually. Current approaches to reduce the burden of malaria include personal protective equipment, curative therapies, and vaccines, though patients are susceptible to repeated, potentially deadly infections throughout their lifetime, because fully protective immunity is not acquired.

To better understand how to treat malaria infections, we need to first understand how the immune system responds to malaria, and how we can manipulate these responses in order to improve them. My research has focused on a type of signaling protein, called cytokines, that are secreted by cells of the immune system, with the focus of this thesis being on CD4⁺ T cells and B cells. B cells present during an infection can survive for years as memory B cells that secrete protective antibodies upon re-encounter with infection, and for this reason are critical to protection against the blood stage of Plasmodium infection, which relies on antibody responses for clearance of infection.

I have found that two cytokines, IL-10 and IL-21, are secreted by CD4⁺ T cells and act upon B cells to support their activation upon infection, and ability to form functional memory B cells.