Abstract
Inflammatory immune responses are necessary for host protection against environmental pathogens. Critical to a successful immune response is the clonal expansion of specific lymphocytes. However, after infection, homeostasis must be returned to the immune system to prevent the development of tissue damage that could lead to autoimmunity. CD95-CD95L-mediated apoptosis is a central component of this process.1 Indeed, mice deficient in functional CD95 or CD95L (lprandgld, respectively) suffer from massive accumulation of lymphocytes and loss of self-tolerance. 2 In addition to reducing lymphocyte numbers, induction of apoptosis is associated with regulation or prevention of inflammatory responses to normal cellular antigens.3
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Elzey, B.D., Ferguson, T.A. (2002). Apoptosis: The Eyes Have It. In: Sullivan, D.A., Stern, M.E., Tsubota, K., Dartt, D.A., Sullivan, R.M., Bromberg, B.B. (eds) Lacrimal Gland, Tear Film, and Dry Eye Syndromes 3. Advances in Experimental Medicine and Biology, vol 506. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0717-8_115
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DOI: https://doi.org/10.1007/978-1-4615-0717-8_115
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