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Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520
Immune responses to infection are optimally designed to generate large numbers of effector T cells while simultaneously minimizing the collateral damage of their potentially lethal actions and generating memory T cells to protect against subsequent encounter with pathogens. Much remains to be discovered about how these equally essential processes are balanced to enhance health and longevity and, more specifically, what factors control effector T cell expansion, differentiation, and memory cell formation. The innate immune system plays a prominent role in the delicate balance of these decisions. Insights into these questions from recent work in the area of effector CD8 T cell differentiation will be discussed.
1 This work was supported by the National Institutes of Health Grants AI066232 and T32 AI055403, the Burroughs-Wellcome Fund Grant 1004313, the Edward Mallinckrodt, Jr. Foundation, the Cancer Research Institute, and the Richard K. Gershon Predoctoral Fellowship.
2 Address correspondence and reprint requests to Dr. Susan M. Kaech, 300 Cedar Street, The Anlyan Center S641B, Yale University School of Medicine, P. O. Box 208011, New Haven, CT 06520. E-mail address: susan.kaech{at}yale.edu
3 Abbreviations used in this paper: KLRG1, killer cell lectin-like receptor; LCMV, lymphocytic choriomeningitis virus; MPEC, memory precursor effector cell; SLEC, short-lived effector cell; TCM, central memory T cell; TEM, effector memory T cell.
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