論文ID: 2024-009
Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a pleiotropic cytokine that differentiates myeloid cells, mediates tissue damage, and regulates immune response. We previously reported a case of systemic lupus erythematosus (SLE) complicated by pulmonary alveolar proteinosis (PAP) with neutralizing anti-GM-CSF antibodies (Ab). In the present study, we examined the existence of anti-GM-CSF Ab in connective tissue disease (CTD), including SLE without PAP, its neutralizing activity, and the associated clinical features.
Subjects were active SLE, dermatomyositis (DM)/polymyositis (PM), and vasculitis. Enzyme-linked immunosorbent assay was developed to detect anti-GM-CSF Ab. The neutralizing activity of anti-GM-CSF Ab was examined to check if it blocked the increase in GM-CSF stimulated CD11b expression on neutrophils. Anti-GM-CSF Ab was detected in the sera from 44/63 (69.8%) SLE, 23/49 (46.9%) DM/PM, and 14/27 (51.8%) vasculitis patients. Neutralizing activity was not detected in sera with anti-GM-CSF Ab from patients with SLE without PAP, DM/PM, and vasculitis. In SLE, the absence of anti-GM-CSF Ab was associated with serum low complement. A possible association was found between the presence of the Ab and pulmonary involvement in SLE. In summary, non-neutralizing anti-GM-CSF Ab was frequently found in connective tissue diseases, including SLE. The association between the antibody and the clinical features in SLE suggested the possibility that non-neutralizing anti-cytokine antibodies could modify the disease phenotype.
