In RA, synovial CXCR6+ TRM cells sustain local inflammation and drive joint damage via chemokine and cytokine outputs; in cutaneous SLE, CCR10-high TRM cells persist in skin and exacerbate local responses through inflammatory mediators; in SSc, perivascular TRM cells may contribute to fibroblast activation and fibrosis (e.g., via TGF-β–linked pathways); and in pSS, glandular CD8+ TRM cells inflict epithelial injury through cytotoxic and inflammatory mechanisms, leading to secretory failure. This evidence concerns the gene CCR10 and rheumatoid arthritis.