CD14+CD11c+HLA-II- monocytes are identified to be associated with osteoclastogenesis in ankylosing spondylitis.

Abnormal monocytes are involved in the pathogenesis of ankylosing spondylitis (AS). We investigated the association between an imbalance of monocyte subpopulations and bone destruction in AS. Compared to controls, AS patients exhibited increased CD14+CD11c+HLA-II- monocytes and decreased CD14+CD11c+HLA-II+ monocytes in peripheral blood. LPS stimulation promoted a shift from CD14+CD11c+HLA-II- monocytes toward CD14+CD11c+HLA-II+ monocytes, enhancing the former's capacity to promote CD4+ T cell proliferation. Micro RNA-seq analysis indicated that AS CD14+CD11c+HLA-II- monocytes were involved in osteoclast differentiation and overproduced soluble osteoclastogenic cytokine CSF-1. In 40 AS patients, evaluated CD14+CD11c+HLA-II- monocytes correlated positively with Spondyloarthritis Research Consortium of Canada (SPARCC) MRI inflammation score (r = 0.336, P = 0.034) and bone erosion score (r = 0.423, P = 0.007), but inversely with ankylosis score (r = -0.346, P = 0.029). Conversely, CD14+CD11c+HLA-II+ monocytes showed the opposite correlation. Our findings demonstrate that expansion of CD14+CD11c+HLA-II- monocytes contribute to bone erosion in AS, potentially mediated through CSF-1-driven osteoclast differentiation.