Tissue resident memory T cells, TRM, represent newly recognized T cell population that play physiologically-relevant role in body's defense against reinfection. TRM cells are local tissue surveyors and act as a first-line defense [alongside of innate immunity] against tissue invading pathogens. Beyond these information nothing much was known about TRM cells.
Using mouse HSV-1 model, the authors found that by day 30 post-infection, Hobit was selectively up-regulated in TRM cells recovered from peripheral tissues, such as skin, but not in central lymphoid tissues such as spleen.
Using Hobit-KO T cells the authors were able to confirm that Hobit was indeed intimately involved in development of tissue-resident memory TRM cells (memory stage, day 40+). Deficiency of another transcription factor, Blimp1, had an additive effect on TRM cells formation when combined with Hobit deficiency.
Interesting, Hobit, in combination with Blimp1, also controlled tissue residency of innate cells such NK and NKT cells.
In summary, this study revealed that transcription factor Hobit controls tissue residency of memory T cells, TRM cells. These data should be considered in developing T cell-oriented vaccines, including cancer immunotherapy (one limitation of this study is that for some reason the authors failed to show actual virus protection data with the regard of Hobit or Hobit + Blimp1 DKO T cells. ).
David Usharauli
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