Tissue-resident memory T (TRM) cells are a recently defined subtype of non-recirculating memory T cells with longevity and protective functions in peripheral tissues. As an essential frontline defense against infections, TRM cells have been reported to robustly patrol the tissue microenvironment in malignancies. Accumulating evidence also implicates that TRM cells in the relapse of chronic inflammatory skin diseases such as psoriasis and vitiligo. In light of these developments, this review aims to synthesize these recent findings to enhance our understanding of TRM cell characteristics and actions. Therefore, after providing a brief overview of the general features of the TRM cells, including precursors, homing, retention, and maintenance, we discuss recent insights gained into their heterogeneous functions in skin diseases. Specifically, we explore their involvement in conditions such as psoriasis, vitiligo, fixed drug eruption - dermatological manifestations of drug reactions at the same spot, cutaneous T cell lymphoma, and melanoma. By integrating these diverse perspectives, this review develops a comprehensive model of TRM cell behavior in various skin-related pathologies. In conclusion, our review emphasizes that deciphering the characteristics and mechanisms of TRM cell actions holds potential not only for discovering methods to slow cancer growth but also for reducing the frequency of recurrent chronic inflammation in skin tissue.
Humans ; Skin Diseases/immunology* ; Memory T Cells/immunology* ; Animals ; Vitiligo/immunology* ; Psoriasis/immunology* ; Immunologic Memory

Objective The abnormal proliferation of renal cells underlies the pathology of progressive glomerulosclerosis.Cell proliferation is regulated by cell regulatory proteins.This study aims to investigate the expression of cyclin-dependent kinase inhibitor P16INK4a in renal tissue of patients with primary mesangial proliferative glomemlonephritis(MsPGN)and its clinical significance.Methods Paraffinembedded renal biopsy renal tissue sections from 36 patients with MsPGN were detected by immunohistochemical staining.Normal renal ti8.Sue sections from 6 nephrectomized patients with trauma were used as controls.Possible correlation between p16 positive area and sclerotic and crescentic glomeruli,blood pressure,serum creatinine,endogenous creatinine clearance rate,and total proteinuria were evaluated.Resuits There were very few expression of P16INK4a in normal glomemli and renal tubular-interstitial.Compared to the normal comrol group,the expression of P16INK4a in 36 renal biopsy specimens with MsPG'N was significantly higher(P<0.01),especially in sclerotic and crescentic glomeruli,and it had wild expression of the same components in no sclerotic and crescentic glomeruli.There was a statistic difference(P<0.01).No statistic difference was found between the expression of P16 INK4a in renal tubular-interstitial of two groups(P>0.05).Therewag positive correlation among P16 INK4a of glomeruli without use of glucocorticoid/immunoinlfibitors and ACEI/ARB(r=0.774,0.497,P<0.01),also blood pressure and 8ul～m creatinine(r=0.64,0.473,P<0.01).It was negstively correlated with endogenous creatinine clearance rate and total proteinuria(r=-0.487,-0.694,P<0.01).There is no correlation between P16INK4s and clinical data in renal tubular-interstitial.Conclusion This study demonstrated that overexpression of P16INK4a in renal tissue with MsPGN may promote the regression ofabnormal proliferation and senescence cells,and induce sclerotic and crescentic glomeruli.The expression level of P16 INK4a not only reflected the degree of renal function,but also hypertension and proteinuria.In brief,expression of P16INK4a may be an important marker in renal sclerotic or crescentic glomeruli of MsPGN.Some drugs may prevent the expression of P16INKa.