Objective To explore the potential pathogenesis of B cells abnormalities in chronic obstructive pulmonary dis-ease(COPD)via analyzing protein-protein interaction(PPI)from single-cell sequencing data.Methods The single-cell sequencing data of peripheral blood mononuclear cells(PBMC)in COPD and rheumatoid arthritis(RA)mice were ob-tained from the Gene Expression Omnibus(GEO)database.The algorithm for dimensionality reduction clustering was used to screened B cells from different clusters with artificial annotation.R Studio was employed to obtain the differential expres-sion genes(DEGs)according to the fold change≥1.2 and P<0.05.The PPI pathways were conducted using the common DEGs between COPD and RA mice.The single-cell sequencing data of human COPD lung tissue were further used for verifying the screened DEGs and PPI pathways from mice.The common DEGs between mice and humans were enriched analyzed by Gene Ontology(GO),Kyoto Encyclopedia of Genes and Ge-nomes(KEGG)and PPI network.Results The common DEGs of B cells between COPD and RA mice were Cd74(log2 FC=0.26,P<0.001),Ctla2a(log2 FC=-0.33,P<0.001),H2-Ab1(log2 FC=0.33,P<0.001),H2-Aa(log2 FC=0.36,P<0.001),Rpl14(log2 FC=0.28,P<0.001),Akap12(log2 FC=-0.58,P<0.001),H2-Eb1(log2 FC=0.42,P<0.001),Bcl2(log2 FC=0.29,P<0.001).The PPI pathways included MHC class Ⅱ molecule-mediated antigen processing and presentation,autoimmune,and lymphocyte activation,respectively.The results were similar in the single-cell sequencing data of human COPD lung tissue,such as the DEGs of CD74(log2 FC=0.80,P<0.001),HLA-DQA1(log2 FC=0.84,P<0.001),HLA-DRB1(log2 FC=0.49,P<0.001)and BCL2(log2 FC=0.40,P=0.034).Compared with the control samples,the proportion of B cells in the human COPD lung tissue was significantly in-creased.Conclusion The enhanced functions of proliferation,activation and antigen presentation in B cells contribute to autoimmune responses,thus leading to the pathogenesis of COPD and irreversible damage of lung tissue.
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