Elevated CDYL expression in the peripheral blood of patients with rheumatoid arthritis.

BACKGROUND

Chromodomain Y-like protein (CDYL), a member of the CDY-related gene family, plays a pivotal role in nervous diseases, reproductive systems and tumors by chromatin remodeling and disrupting normal transcriptional regulation. However, the expression and biological functions of CDYL in rheumatoid arthritis (RA) remain unclear. This study aims to investigated the role of CDYL in the pathogenesis of RA.

METHODS

A cohort of 43 RA patients and 36 healthy subjects were included in the study. The transcript levels of CDYL, interleukin-17 A (IL-17 A) and IL-22 were detected by quantitative real-time PCR. Flow cytometry and Western blot were used to analyze the relationship between CDYL and Th17 cells. The GSE100191 dataset from the GEO database was downloaded to conduct a comprehensive bioinformatics analysis of the potential functions of CDYL. The interaction of CDYL and EZH2 and the effects of the EZH2 antagonist on Th17 cells were measured by Western blot.

RESULTS

The CDYL was highly expressed in the PBMCs derived from RA patients, exhibiting positive correlations with DAS28 score (r = 0.36, p < 0.0177) and serum anti-cyclic citrullinated peptide antibody titers (r = 0.4255, p = 0.004). Moreover, the transcript levels of CDYL were positively correlated with elevated IL-17 A levels (r = 0.5140, p < 0.001) and IL-22 (r = 0.4540, p = 0.002) levels in RA patients and the RA dataset. CDYL expression is markedly upregulated in Th17 cells, while the proportion of Th17 cells is increased in RA patients. Mechanistically, CDYL knockdown significantly inhibited Th17 differentiation in vitro, which suggests that CDYL is associated with and functionally contributes to the differentiation of Th17 cells.

CONCLUSIONS

Our findings indicate that CDYL expression is associated with and promotes the differentiation of Th17 cells in RA patients and may be involved in the process of RA.