In:
The Journal of Immunology, The American Association of Immunologists, Vol. 206, No. 1_Supplement ( 2021-05-01), p. 98.25-98.25
Abstract:
The memory T cell population must be durable and capable of responding with rapid effector functions during re-encounter with pathogens. This is accomplished by forming a memory CD8 T cell pool containing multiple distinct subsets of cells that combine varying functional and homing characteristics. At steady-state, memory T cells expressing KLRG1 are restricted to circulation and patrol the host from within the vasculature. These cells convey robust protection during acute rechallenge with pathogens delivered intravenously. Given their localization pattern, we questioned whether KLRG1+ memory T cells participate in immune responses within non-lymphoid tissues. Here, we find that during local and systemically administered infections, KLRG1+ memory cells alter their trafficking pattern and enter infected non-lymphoid tissues. Following intranasal influenza infection, antigen-specific KLRG1+ memory cells proliferate and extravasate into the lung parenchyma. Additionally, during acute LCMV infection, similar findings were observed in all non-lymphoid tissues assayed, including small intestine, kidney, and salivary gland, indicating this is not a unique phenomenon, but rather a consistent trait of these cells. Unexpectedly, progeny from KLRG1+ cells remained within non-lymphoid tissues after acute infection is cleared, downregulating markers of circulation (CX3CR1, KLRG1) and acquiring markers of tissue residency (CD69, CD103). This work challenges the concept that KLRG1+ memory cells are terminally differentiated and demonstrates unappreciated plasticity within this subset to support immunity within non-lymphoid tissues.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.206.Supp.98.25
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2021
detail.hit.zdb_id:
1475085-5
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