The clonal selection theory that “a lymphocyte expresses only one receptor” [1]has been challenged and complemented by “dual TCR αβ T cells” [2]. “Dual-receptor lymphocytes” are closely related to the mechanisms of self-tolerance and response, as well as the onset and progression of autoimmune diseases [3], [4].

Ankylosing spondylitis(AS) is a spinal and sacroiliac joint inflammatory disease predominantly resulting in abnormal bone remodeling and ankylosis, often accompanied by intestinal inflammation and uveitis. Its pathogenesis has been linked to a variety of factors, including genetic predisposition, immunological abnormality, and gut microbes [5]. A variety of experimental evidence suggests that T cells are involved in the onset and progression of AS. For example,clonal expansion of CD8+ T cells is present in patients harboring the HLA-B*27 susceptibility gene [6], elevated Th17 frequency [7], effectiveness of anti-interleukin-17A monoclonal antibody (secukinumab) therapy [8], reduced Treg cell ratio and functional defects are also found in AS patients [9]. However, TCR characterization of T cells in AS remains elusive. Recently, Kijong et al. identified and demonstrated the involvement of TNFRSF4+ (OX40) and TNFRSF18+ (GITR) Th17 (pTh17) cells in AS synovial tissue inflammation and pathogenesis .In this study, based on the mechanism of dual TCR T cells in autoimmune diseases [3], [4], and dual TCR Th17 mediated inflammatory response in humans and mice [11].We used scRNA + TCR-seq technology to elucidate TCR pairing [12]. It was the first time to find that there was a high proportion of dual TCR-type memory CD4+/CD8+ T, pTh17 and Treg in AS patients, and there was characteristic transcription factor expression and a high proportion of CDR3 overlap in AS patients. All these results indicate that dual TCR-T cells may participate in the autoimmune response of AS patients.