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Abstract
ObjectiveCirculating follicular helper T (cTfh) cells are a specialized subset of CD4+ T cells that express the CXC-chemokine receptor 5 (CXCR5). These cells exhibit immune activities by inducing B cell differentiation and proliferation via the secretion of interleukin (IL)-21. Multiple studies have demonstrated that cTfh cells are associated with the progression and severity of numerous diseases. To investigate the role of cTfh cells in the development of Kawasaki disease (KD), we analyzed the distinct subpopulations of cTfh cells and serum IL-21 levels in different phases of KD.MethodsAccording to the differential expression of inducible co-stimulator (ICOS) and programmed cell death protein 1 (PD-1), cTfh cells were divided into distinct subsets. We used flow cytometry and flow cytometric bead arrays (CBA) to analyze subsets of CD4+CXCR5+ T cells and serum IL-21 levels. The samples were collected from control subjects and Kawasaki disease patients in the acute and remission phases.ResultsIn the acute phase (AP), the percentages of ICOShighPD-1high, ICOS+PD-1+, ICOS−PD-1+, CD45RA−IL-21+ cTfh cells and serum IL-21 levels significantly increased. Furthermore, the percentages of ICOShighPD-1high and ICOS+PD-1+ cTfh cells positively correlated with erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) values, whereas the percentage of ICOS−PD-1+ cTfh cells indicated negative correlations. The percentages of ICOS+PD-1+, ICOShighPD-1high and CD45RA−IL-21+ cTfh cells correlated positively with serum IL-21 levels. In the remission phase (RP), the percentages of ICOS−PD-1+, CD45RA−IL-21+ cTfh cells and serum IL-21 levels were significantly decreased. In contrast, the percentages of ICOS+PD-1+, ICOShighPD-1high, and ICOS+PD-1− cTfh cells were further increased. Among these subsets, only CD45RA−IL-21+ cTfh cells correlated positively with serum IL-21 levels.ConclusionsThe present study is the first investigation that examined the distribution of circulating cTfh cell subsets in Kawasaki disease. Both cTfh cells and serum IL-21 are essential to the pathogenesis of KD. Our study provides further understanding of the immune response involved in KD and offers novel insights in the pathogenetic mechanism of this disease.
Highlights
Kawasaki disease (KD) is an acute febrile vasculitis that was first reported in 1967 [1]
The present study is the first investigation that examined the distribution of circulating Circulating follicular helper T (cTfh) cell subsets in Kawasaki disease
Our study provides further understanding of the immune response involved in KD and offers novel insights in the pathogenetic mechanism of this disease
Summary
Kawasaki disease (KD) is an acute febrile vasculitis that was first reported in 1967 [1]. Both innate and adaptive immune systems are involved in the pathogenesis of KD. T cells have traditionally been considered to play essential roles in adaptive immune responses, the alterations in the percentage of T cells in KD are a subject of controversy and different investigators have reported conflicting results [8,9,10]. Current studies that examined the variation of T-cell subpopulations with regard to KD have generally investigated T helper cells [11, 12], regulatory T cells [13], and cytotoxic T cells [14]; the role of follicular helper T (Tfh) cells in KD remains to be elucidated. The studies conducted on Tfh cells are important in clarifying the role of B cells in KD, since Tfh cells can aid the function of B cells
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