Abstract
AimIgA-producing B cells have been found to be associated with children diagnosed with Henoch-Schonlein purpura (HSP). The aim of the present study was to determine whether children with HSP possess altered B-cell subsets.MethodsA total of 14 children diagnosed with HSP and age- and sex-matched healthy controls (HCs) were enrolled in our study. Peripheral blood mononuclear cells were isolated, and the percentage and absolute number of B-cell subsets and Follicular helper T (Tfh) cells were determined by flow cytometry. Finally, Spearman’s correlation coefficient was used to analyse the correlation between the percentage of Tfh cells and B-cell subsets.ResultsWe found that compared to HCs, the frequency and absolute number of total B cells were significantly higher in children with HSP, but the percentages of plasma cells and naïve B cells were significantly lower. A significantly increased percentage and absolute number of memory nonswitched B cells were found in children with HSP compared with HCs. We observed that the expression of C-X-C chemokine receptor type 5 (CXCR5) on total CD4+ T cells and the percentage of CD4+CXCR5+ cells were significantly increased in patients with HSP. Moreover, significantly correlations between Tfh cells and various B-cell subsets were observed.ConclusionsOur study showed a Tfh-cell-associated altered B cell compartment in children with HSP.
Highlights
Henoch-Schonlein purpura (HSP), the most common type of childhood vasculitis, is characterized by the deposition of systemic IgA immune complexes in the walls of small vessels [1]
Significant correlations were found between T follicular helper (Tfh) cells and B-cell subsets
Increased IgA indicates that humoral immunity underlies the manifestations of HSP; whether altered proportions of B-cell subsets and Tfh-dependent B cell responses play a role in the pathogenesis of HSP remains unknown
Summary
Henoch-Schonlein purpura (HSP), the most common type of childhood vasculitis, is characterized by the deposition of systemic IgA immune complexes in the walls of small vessels [1]. It is estimated that 1/5000 children acquire HSP per year [2]. Considered to be a self-limiting condition, HSP is manifested by skin purpura, arthritis, abdominal pain and renal involvement, and the exact pathogenesis of HSP remains unknown. HSP is a systemic inflammatory disease that is characterized by leucocyturia, haematuria and proteinuria. Inflammatory cytokines, such as interleukin (IL)-6, IL-10 and IL-17, have been reported to be involved in the pathogenesis of HSP[3,4,5].
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