CD69 suppresses response to the S1P chemoattractant from blood and lymph and prevents TRM cells from exiting peripheral tissue.
The main role in formation of TRM cells has CD103 and expression of this integrin is dependent on the cytokine TGF-β.
[19][20][21] Also, generation of CD103+ TRM cells requires low expression of Eomes and T-bet transcription factors.
[9] TRM cells reside in many tissues that create barriers against outside environment and thus provide defense against repeatedly incoming pathogens.
In the skin, lung, brain, and vagina TRM cells are required to provide immediate rapid control of re-infection.
[5] TRM cells express granzyme B which helps limit the spread of pathogens at the site of infection.
Whereas large fraction of TILs are TRM cells, they are candidates for solid cancer immunotherapy.
They have decreased expression of IFN-ɤ, TNF-α and IL-2 in comparison with circulating T cells in melanoma patients what suggest different mechanism for tumor growth control.
This suggests, that most of the tumor TRM show an exhausted phenotype which may be saved by immune checkpoint inhibitor therapies.
Multiple genes as well as environment play role in developing vitiligo and migration of CD8+ T cells correlates with the state of disease.
There is also higher number of CD49a+ CD8+ CD103+ T cells with cytotoxic potential in epiderma and derma of the vitiligo patients in comparison with healthy skin.
TRM cells have reduced IFNɤ production and white spots on skin disappear.