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IL-2 is required for the generation of viral-specific CD4+ Th1 tissue-resident memory cells and B cells are essential for maintenance in the lung.

Brian D HondowiczKaren S KimMikel J RuterbuschGladys J KeitanyMarion Pepper
Published in: European journal of immunology (2017)
CD4+ tissue resident cells are an important first line of defense against viral infections in the lungs and are critical for promoting the localization of lung resident CD8+ T cells. However, relatively little is known about the signaling programs required for the development of viral-specific CD4+ tissue resident cells in the lungs. Recently, it was shown that signaling through the high affinity IL-2 receptor is required for the differentiation of lung-resident Th2 memory (Trm) cells in a murine model of airway inflammation. We therefore tested if IL-2 signaling is also required for the development of viral antigen-specific CD4+ Th1 cells in the lung after i.n. infection with lymphocytic choriomeningitis virus. These studies demonstrate that Th1 CD4+ T cells also require IL-2 for lung Trm development. Additionally, they show that B cells potently inhibit early Th1 cell lung residency, but are required for the maintenance of a long-lived population of CD4+ Th1 Trm.
Keyphrases
  • induced apoptosis
  • cell cycle arrest
  • sars cov
  • patient safety
  • quality improvement
  • endoplasmic reticulum stress
  • signaling pathway
  • nk cells
  • working memory
  • pi k akt
  • binding protein