Journal
JOURNAL OF IMMUNOLOGY
Volume 203, Issue 4, Pages 936-945Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1900093
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Funding
- National Institutes of Health (NIH) [K22 AI110581]
- NIH [R01 AI132962, T32 HL007741, T32 AI007313]
- National Institute of Allergy and Infectious Diseases, the NIH
- Department of Health and Human Services under Centers of Excellence for Influenza Research and Surveillance Contract [HHSN272201400005C]
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Resident memory T cells (T-RM) in the lung are vital for heterologous protection against influenza A virus (IAY). Environmental factors are necessary to establish lung T-RM; however, the role of T cell-intrinsic factors like TCR signal strength have not been elucidated. In this study, we investigated the impact of TCR signal strength on the generation and maintenance of lung T-RM after IAV infection. We inserted high- and low-affinity OT-I epitopes into IAV and infected mice after transfer of OT-I T cells. We uncovered a bias in T-RM formation in the lung elicited by lower affinity TCR stimulation. TCR affinity did not impact the overall phenotype or long-term maintenance of lung T-RM. Overall, these findings demonstrate that T-RM formation is negatively correlated with increased TCR signal strength. Lower affinity cells may have an advantage in forming T-RM to ensure diversity in the Ag-specific repertoire in tissues.
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