Characteristics of B cell‑associated gene expression in patients with coronary artery disease.

The current study aimed to identify differentially expressed B cell‑associated genes in peripheral blood mononuclear cells and observe the changes in B cell activation at different stages of coronary artery disease. Groups of patients with acute myocardial infarction (AMI) and stable angina (SA), as well as healthy volunteers, were recruited into the study (n=20 per group). Whole human genome microarray analysis was performed to examine the expression of B cell‑associated genes among these three groups. The mRNA expression levels of 60 genes associated with B cell activity and regulation were measured using reverse transcription‑quantitative polymerase chain reaction. The mRNA expression of the B cell antigen receptor (BCR)‑associated genes, CD45, NFAM, SYK and LYN, were significantly upregulated in patients with AMI; however, FCRL3, CD79B, CD19, CD81, FYN, BLK, CD22 and CD5 mRNA expression levels were significantly downregulated, compared with patients in the SA and control group. The mRNA levels of the T‑independent B cell‑associated genes, CD16, CD32, LILRA1 and TLR9, were significantly increased in AMI patients compared with SA and control patients. The mRNA expression of genes associated with T‑dependent B cells were also measured: EMR2 and CD97 were statistically upregulated, whereas SLAMF1, LY9, CD28, CD43, CD72, ICOSL, PD1, CD40 and CD20 mRNAs were significantly downregulated in AMI group patients compared with the two other groups. Additionally the gene expression levels of B cell regulatory genes were measured. In patients with AMI, CR1, LILRB2, LILRB3 and VAV1 mRNA expression levels were statistically increased, whereas, CS1 and IL4I1 mRNAs were significantly reduced compared with the SA and control groups. There was no statistically significant difference in B cell‑associated gene expression levels between patients with SA and the control group. The present study identified the downregulation of genes associated with BCRs, B2 cells and B cell regulators in patients with AMI, indicating a weakened T cell‑B cell interaction and reduced B2 cell activation during AMI. Thus, improving B2 cell‑mediated humoral immunity may be a potential target for medical intervention in patients with AMI.