We also detected increased receptors in TREM2+ MФs receiving signals from other cells were involved in cell survival, phagocytosis, and calcium homeostasis via TNFR2 (Tnfrsf11b)-GRN, MET-SEMA4D/SEMA5A, CD48-CD2/CD244, FCGR1-BGP (Ceacam1), CD180-LY86, CXCR4-CXCL12, IL4RA-IL13 R-L interactions; and decreased receptors resulting in the dysregulation of coagulation and complement activation corresponding to fibrosis and hypercoagulative state in SSc (e.g., CD36-THBS1/COL1A1/SAA1, IL17RA-IL17A/IL17F, C5AR1-RPS19/GNAIL2) (Figure 3F, Supplementary Table S9). This evidence concerns the gene SEMA4D and systemic sclerosis.