😲🤩 Has a name yet??

Thank u & great to connect again here Cliona! Indeed we've wondered then sifted through still-quite-conflicting lit on CD1dKOs, pre vs post activated NKT cells in hepatectomy. Also maybe functional subsets/lineages can compensate & muddle the phenotype, we could knock more of'em out simultaneously..

Many thanks to our collaborators across Unimelb MDHS, The Florey Institute, University of Queensland, Austin Health for providing tools, resources and discussion towards this study!

Conceptually, non-peer review'd diagram here: Within T cells at least, integrating thoughts posed by labs of P.Brennan, B.Jabri, perhaps the extent of tissue damage sensitivity could be a hallmark of the ‘T cell-innateness’ theory. tinyurl.com/ycy6dv24
tinyurl.com/bd6kxekk

Overall, these have implications to how we should (in certain contexts) move away from studying our T cell lineages in isolation, and the role of T cell IL-4 production that is now getting resurged attention.

Towards discussion, this sensing of damage metabolites may act to prevent excessive tissue inflammation and injury as a way to maintain tissue homeostasis from the explosive cytokine production from these innate-T cells, UNTIL there is cognate antigen for them involved.

Our data indicates that upon insult, release of tissue damage metabolites drives this P2RX7-mediated depletion of T-bet+ innate-T cells. Blocking this also uncovered more numbers & subsets (CD4 innate-like IFNg/IL-4++ anyone?) than we thought originally exists. Also raising the q of 'why them'?

This all started in the quest of trying to recover enough numbers of NKT/MAIT/gdT cells ex vivo, why do (some) of them die so easily?? We followed the literature & the correlation of P2RX7 (not other P2RX's) expression on innate-like T cells was a key, in both mice and humans.