Immune Response of β2-Microglobulin-Deficient Mice to Pathogens
The ability of hosts to respond to pathogens is one of the driving forces in the selection of the immune system. The immune response to both bacteria and viruses involves the ability of T cell to recognize and to respond to pathogens. Both CD4+ and CD8+ T cells are important in the overall immune response. In the most basic paradigm, CD4+ T cells respond to exogenous antigen, which is internalized, degraded, and presented on the surface of antigen-presenting cells by major histocompatibility complex (MHC)-encoded class II molecules. This arm of the response includes not only helping B cells produce antibodies, but also the production of proinflamatory cytokines, including interferon (INF)-γ, tumor necrosis factor (TNF)-α, and interleukin (IL)-2. It is often stated that these responses are important in inhibiting the spread of virus from cell to cell by aiding the production of antibodies which neutralize virus and creating a cytokine milieu which does not support virus replication. In contrast, CD8+ T cells respond primarily to peptides derived from endogenously synthesized proteins. The T cells are able to recognize and kill the cells expressing these peptides by at least two major pathways, one utilizing perforin exocytosis and the other utilizing fas-fas ligand interactions. This response has the net effect of removing cells which are producing viruses or other pathogens which have access to the cytoplasm of infected cells. This has given rise to the simple idea that CD4 responses (and antibodies) block virus spread, while CD8 responses remove the source of infection, resulting in clearance of pathogens which hide intracellularly.
KeywordsMajor Histocompatibility Complex Major Histocompatibility Complex Class Mouse Hepatitis Virus Lymphocytic Choriomeningitis Virus Listeria Monocytogenes Infection
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