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• W2040984333 abstract "Whether differences between naive cell-derived primary (1°) and memory cell-derived secondary (2°) CD4(+) T-cell effectors contribute to protective recall responses is unclear. Here, we compare these effectors directly after influenza A virus infection. Both develop with similar kinetics, but 2° effectors accumulate in greater number in the infected lung and are the critical component of memory CD4(+) T-cell-mediated protection against influenza A virus, independent of earlier-acting memory-cell helper functions. Phenotypic, functional, and transcriptome analyses indicate that 2° effectors share organ-specific expression patterns with 1° effectors but are more multifunctional, with more multicytokine (IFN-γ(+)/IL-2(+)/TNF(+))-producing cells and contain follicular helper T-cell populations not only in the spleen and draining lymph nodes but also in the lung. In addition, they express more CD127 and NKG2A but less ICOS and Lag-3 than 1° effectors and express higher levels of several genes associated with survival and migration. Targeting two differentially expressed molecules, NKG2A and Lag-3, reveals differential regulation of 1° and 2° effector functions during pathogen challenge." @default.
• W2040984333 created "2016-06-24" @default.
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• W2040984333 date "2012-08-27" @default.
• W2040984333 modified "2023-10-05" @default.
• W2040984333 title "Memory CD4⁺T-cell–mediated protection depends on secondary effectors that are distinct from and superior to primary effectors" @default.
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• W2040984333 doi "https://doi.org/10.1073/pnas.1205894109" @default.
• W2040984333 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3458385" @default.
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