IntroductionKawasaki disease (KD) , also known as Kawasaki syndrome, is an acute, self-limited febrile vasculitis that predominantly affects infants and children under 5 years of age [1]. KD is characterized by high spiking fever persisting for more than 5 days, erythematous rash, bilateral conjunctivitis, congestive oral mucosa, swelling lymph node, and edematous extremity [2]. Furthermore, KD is the most common cause of acquired cardiac disease, especially coronary artery aneurysms in children [3]. Although KD has been studied for almost half a century, the pathogenic mechanism of KD remains unclear. Furthermore, while most patients respond well to intravenous immunoglobulin (IVIG), roughly one-quarter of the children meeting clinical criteria will go on to have coronary artery inflammation, including aneurysms [4]. Hence, further illustration of the mechanism of KD is a crying need to find a therapeutic for KD treatment clinically.Both innate and adaptive immune systems are involved in the pathogenesis of KD [5]. The early event of visualized immunological abnormality is the activation of innate immune system represented as the elevated numbers of activated monocytes and increased expression of circulating cytokines, such as interleukin (IL)-6 and tumor necrosis factor (TNF) -α [6]. Subsequently, it is generally believed that autoreactive T cell and their inflammatory cytokines play a major role in the development of KD [7]. T helper (Th) 17 cells, a recently identified lineage of CD4+ Th cells, predominantly produce IL-17A. Th17 cell and IL-17A have been shown to participate in host defense responses and inflammatory diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Graves’ disease (GD), and Crohn’s disease (CD) [8-11]. A recent study has shown that a high frequency of Th17 cells and high levels of IL-17 were demonstrated in the acute stage of KD, and that elevated Th17 cells might be associated with tissue damage and coronary artery aneurysm formation [7, 12]. However, there is little information about whether higher frequency of Th17 and higher concentrations of IL-17A also exist in Chinese patients with KD and how Th17 responses are associated with the development of coronary artery aneurysm in KD patients.More notably, a newly identified T-cell subset, termed Th22 cells, has been described as expressing their key cytokines interleukin (IL)-22, which can activate signal transduction and transcription 3 (STAT3) [13]. IL-22, originally termed as an IL-10-related T-cell-derived-inducible factor, enhance innate immunity and promote epithelial cell proliferation and tissue. In contrast, IL-22 also act as regulator in the pathogenesis of RA and SLE [14-15]. Furthermore, recent studies have reported that IL-22 may function as a biphasic cytokine: protective and regenerative in steady state while amplifying proinflammatory signals given by TNF-α [16], which is necessary for exacerbation of vascular injury in KD. However, little is known about the role of Th22 cells in the pathogenesis of KD. We believe that Th22 cells may partially contribute to the formation of coronary aneurysms.Here, in the current study, we sought to further clarify the mechanism underlying hyperactivation of Th22 and Th17 during acute KD. We characterized the numbers of circulating Th22 and Th17 cells by flow cytometry, and measured the concentration of serum inflammatory cytokines by enzymelinked immunosorbent assay (ELISA) in 43 Chinese patients with new onset KD. Furthermore, we analyzed the potential association of the numbers of Th22 and Th17 cells with the clinical measures in these KD patients. Our findings indicated that increased numbers of Th22 and Th17 cells might be contributed to the pathogenesis of KD in Chinese patients.