Journal
NATURE IMMUNOLOGY
Volume 12, Issue 6, Pages 485-491Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2029
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Funding
- NIAID NIH HHS [R01 AI076457-04, R01 AI041576, R01 AI041576-14, R01 AI076457, R01 AI041576-15, P01 AI056172, P01 AI056172-07] Funding Source: Medline
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After infection, most antigen-specific memory T cells reside in nonlymphoid tissues. Tissue-specific programming during priming leads to directed migration of T cells to the appropriate tissue, which promotes the development of tissue-resident memory in organs such as intestinal mucosa and skin. Mechanisms that regulate the retention of tissue-resident memory T cells include transforming growth factor-beta (TGF-beta)-mediated induction of the E-cadherin receptor CD103 and downregulation of the chemokine receptor CCR7. These pathways enhance protection in internal organs, such as the nervous system, and in the barrier tissues-the mucosa and skin. Memory T cells that reside at these surfaces provide a first line of defense against subsequent infection, and defining the factors that regulate their development is critical to understanding organ-based immunity.
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