Journal
IMMUNITY
Volume 41, Issue 4, Pages 633-645Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2014.09.007
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Funding
- NIH [RO1AI066232, R01AI074699, R01AR40072, P30AR053495, R21AR063942, T32AI07019, F31AG07777]
- Howard Hughes Medical Institute
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Tissue-resident memory T (Trm) cells provide enhanced protection against infection at mucosal sites. Here we found that CD4(+) T cells are important for the formation of functional lung-resident CD8(+) T cells after influenza virus infection. In the absence of CD4(+) T cells, CD8(+) T cells displayed reduced expression of CD103 (Itgae), were mislocalized away from airway epithelia, and demonstrated an impaired ability to recruit CD8(+) T cells to the lung airways upon heterosubtypic challenge. CD4(+) T cellderived interferon-gamma was necessary for generating lung-resident CD103(+) CD8(+) Trm cells. Furthermore, expression of the transcription factor T-bet was increased in unhelped lung Trm cells, and a reduction in T-bet rescued CD103 expression in the absence of CD4(+) T cell help. Thus, CD4(+) T cell-dependent signals are important to limit expression of T-bet and allow for the development of CD103(+) CD8(+) Trm cells in the lung airways following respiratory infection.
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