Immunopathology

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Abstract

Immune responses to viral infections are generated by the host in order to survive and ideally to eliminate the virus. These robust antiviral immune responses also by design cause tissue damage. Antibodies react with virus and viral antigens in the fluid phase forming virus-antibody immune complexes that deposit in mesangial cells and macrophages. Cytotoxic T cells are designed to kill cells that make viral progeny thus removing the factories that produce infectious progeny. Indeed, most symptoms accompanying viral infections are caused by these actions and the release of cytokines and chemokines. When the balance of immunity is shifted to excess then immunopathology occurs. That is, the virus-antibody immune complexes overload the mesangial area and deposit in glomeruli and arteries causing kidney disease and arteritis. T cells cause multiple injuries to liver, heart, brain, as well as other tissues. Primarily, not only the adaptive immune system but also the innate immune system is responsible for the immunopathology. Overall, early recognition of viral infection is paramount for viral clearance and/or immunopathology by the adaptive immune system. Cells of the innate immune system are primarily responsible for transporting virus/viral antigens from the sites of infection to the draining lymph nodes where the cells can 'present' viral peptides and activate cells of the adaptive immune system. Therefore, the two immune systems are intimately linked. Components of the adaptive immune system which are responsible for tissue damage/immunopathology are CD4+ and CD8+ T cells, as well as B cells. Generally, immune responses to viruses that are noncytolytic or have relatively low cytolytic potential can result in extensive cell death or tissue destruction. Cytolytic viruses also induce immunopathologic injury but in addition cause injury by apoptosis or membrane-membrane fusion (syncytia formation).

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Oldstone, M. B. A., & Fujinami, R. S. (2008). Immunopathology. In Encyclopedia of Virology (pp. 78–83). Elsevier Ltd. https://doi.org/10.1016/B978-012374410-4.00592-6

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