Adaptive Immunity to Parasites

Cell-Mediated

Although the innate immune system provides an effective first line of defence, T cells are fundamental in the development of immunity, demonstrated using T-cell deprived mice that fail to resolve otherwise non-lethal infections of, for example, T. cruzi.

• Both CD4⁺ and CD8⁺ cells are required for protection, e.g CD4⁺ cells protect against the blood stage of a Plasmodium infection (erythrocytes do not express MHC class I), while CD8⁺ cells are required to mediate immunity against the liver stage (hepatocytes do not express MHC class II).
• T_H1 cells are required to fight intracellular protozoa - the release of Interferon-γ (IFNγ) activates macrophages to kill the protozoa residing within them
• Helminth infections require both T_H1 and T_H2 responses, e.g. during S. mansoni the secretion of IFNγ by T_H1 cells activates mechanisms that destroy larvae in the lungs, although the T_H2 subset, secreting Interleuken-5 (IL-5), predominate. IL-5 is the cytokine responsible for the eosinophilia associated with parasite infections.
• T_H2 cells are required for the destruction of intestinal worms, where they induce mucosal mast cells and interact with eosinophils

Humoral

While cell-mediated immunity is important in tissue infections, such as Leishmania, specific antibodies are important in controlling parasites that live in the bloodstream, e.g. malaria. Mechanisms of antibody-mediated immunity include:

• Directly damaging protozoa
• Activating complement, and the subsequent Membrane Attack Complex
• Blocking attachment to host cells
• Enhancing macrophage phagocytosis
• Involvement in antibody-dependent cell-mediated cytotoxicity

The humoral response involves the production of IgE. It is stimulated by mast cells producing IL-4 (innate response). It also includes isotype switching of B cells to produce IgE.

Also see Immunity to Parasites

Originally funded by the RVC Jim Bee Award 2007