Complement Innate Immune

Gene co-expression module in Endothelial

View this module in SCUBA

Why this annotation

Hub genes C1R and C1S (serine proteases of the complement C1 complex, classical pathway initiation), CTSS (cathepsin S, lysosomal protease for MHC-II antigen processing and complement activation), TAPBP (tapasin, MHC-I peptide loading complex), GSDMD (gasdermin D, pyroptosis effector), OPTN (optineurin, NF-κB/autophagy regulator), LGALS9 (galectin-9, immune checkpoint ligand), TYMP (thymidine phosphorylase, inflammatory angiogenesis), TNIP1 (ABIN-1, ubiquitin-binding NF-κB inhibitor), and MFGE8 (milk fat globule EGF factor 8, efferocytosis). The combination of complement initiation (C1R/C1S), antigen presentation machinery (CTSS/TAPBP), and cell death effectors (GSDMD) defines an innate immune sensing and complement activation program in inflamed endothelium. Upregulated in IBD inflammation, reversed in remission. Neighbor to M61 (NF-κB) and M58 (coagulation), representing the complement/innate immune arm of the inflammatory response.

Genes

C1R, C1S, CD47, CNDP2, COL5A2, CTSS, GRINA, GSDMD, LGALS9, MFGE8, NUB1, OPTN, RBCK1, RELL1, SQOR, TAPBP, TNIP1, TYMP

Most correlated modules

• Leukocyte Recruitment Signaling · correlation 0.81
• Lysosomal Autophagy Program · correlation 0.81
• Procoagulant TGF-β Response · correlation 0.76
• Inflammatory Stress Response · correlation 0.76
• NF-κB Endothelial Activation · correlation 0.73
• IFN-gamma Response · correlation 0.68
• Myeloid Contamination · correlation 0.66
• Endothelial Quiescence Identity · correlation 0.66

Module annotations were drafted by a large language model from the module's genes, then reviewed and approved by a domain expert. See sources & licences.