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J Immunol Res. 2026;2026(1):e2743928. doi: 10.1155/jimr/2743928.

ABSTRACT

OBJECTIVES: This study aimed to systematically investigate the dynamics changes in membrane-bound B7-H4 (mB7-H4) expression and soluble B7-H4 (sB7-H4) levels in the peripheral blood of patients with acetylcholine receptor antibodies (AchR-Ab)-positive myasthenia gravis (MG) across different disease phases, and to explore their clinical significance.

METHODS: AchR-Ab-positive MG patients at baseline, relapse, and remission stages, along with age- and sex-matched healthy controls (HCs), were enrolled. Peripheral blood was obtained from all participants. mB7-H4 expression on circulating immune cell subsets was determined by flow cytometry, while plasma sB7-H4 concentration was quantified using enzyme-linked immunosorbent assay (ELISA).

RESULTS: Compared to HC, patients with relapsing MG exhibited significantly increased mB7-H4 expression on CD4+ T cells and CD14+ monocytes (p < 0.05). In contrast, plasma sB7-H4 levels were markedly decreased in relapsing-MG patients relative to HC (p < 0.05). Among MG subgroups, mB7-H4 expression on CD4+ T cells was significantly higher in relapsing-MG patients than in those at baseline or in remission (p < 0.05). Conversely, plasma sB7-H4 levels were significantly lower in both relapsing and remitting patients compared with the baseline-MG group (p < 0.05). Within the relapsing-MG patients, patients with abnormal thymic pathology exhibited significantly lower sB7-H4 levels than those with a normal thymus (p < 0.05). Correlation analyses demonstrated that mB7-H4 expression on CD14+ monocytes was positively correlated with quantitative MG scores (QMGs; r = 0.544, p = 0.020), whereas sB7-H4 levels were negatively correlated with QMGs (r = -0.417, p = 0.016). Immunosuppressive treatment did not significantly affect sB7-H4 levels compared with pre-treatment values (p > 0.05). Univariate analysis identified elevated mB7-H4 expression on CD4+ T cells as a potential risk factor for MG relapse. However, this association did not remain significant after multivariate adjustment for confounders variables.

CONCLUSIONS: During MG relapse, inflammatory activation may engage the B7-H4 pathway, characterized by increased mB7-H4 and decreased sB7-H4 levels, which may cooperatively contribute to immune suppression and serve as a compensatory protective mechanism. B7-H4 expression appears to be associated with disease severity. Thymic abnormalities may contribute to the downregulation of sB7-H4, whereas immunosuppressive treatment may not significantly modify its circulating levels. Although increased CD4+ B7-H4 expression is associated with relapse, it does not represent an independent predictor of relapse risk.

PMID:42106024 | DOI:10.1155/jimr/2743928


Source: https://pubmed.ncbi.nlm.nih.gov/4210602 ... 4&v=2.20.0