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Secondary infections rejuvenate the intestinal CD103+ tissue-resident memory T cell pool

Science Immunology article from the Zehn lab (B14)

04.11.2022


Madlaina von Hoesslin, Miriam Kuhlmann , Gustavo Pereira de Almeida, Kristiyan Kanev, Christine Wurmser , Ann-Katrin Gerullis , Patrick Roelli, Jacqueline Berner and Dietmar Zehn (4 Nov 2022) Secondary infections rejuvenate the intestinal CD103+ tissue-resident memory T cell pool. Science Immunology 7(77). DOI: 10.1126/sciimmunol.abp9553 (Project B14)


Abstract cited from the article:

Resident T lymphocytes (TRM) protect tissues during pathogen reexposure. Although TRM phenotype and restricted migratory pattern are established, we have a limited understanding of their response kinetics, stability, and turnover during reinfections. Such characterizations have been restricted by the absence of in vivo fate-mapping systems. We generated two mouse models, one to stably mark CD103+ T cells (a marker of TRM cells) and the other to specifically deplete CD103− T cells. Using these models, we observed that intestinal CD103+ T cells became activated during viral or bacterial reinfection, remained organ-confined, and retained their original phenotype but failed to reexpand. Instead, the population was largely rejuvenated by CD103+ T cells formed de novo during reinfections. This pattern remained unchanged upon deletion of antigen-specific circulating T cells, indicating that the lack of expansion was not due to competition with circulating subsets. Thus, although intestinal CD103+ resident T cells survived long term without antigen, they lacked the ability of classical memory T cells to reexpand. This indicated that CD103+ T cell populations could not autonomously maintain themselves. Instead, their numbers were sustained during reinfection via de novo formation from CD103− precursors. Moreover, in contrast to CD103- cells, which require antigen plus inflammation for their activation, CD103+ TRM became fully activated follwing exposure to inflammation alone. Together, our data indicate that primary CD103+ resident memory T cells lack secondary expansion potential and require CD103− precursors for their long-term maintenance.


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