Characteristics of immune function in the acute phase of Henoch-Schönlein purpura

Henoch-Schönlein purpura (HSP) is still diagnosed using symptoms and signs together with some histopathological findings. The purpose of this study was to summarize the characteristics and roles of cellular and humoral immunity in children with Henoch-Schönlein purpura (HSP).

A total of 502 cases of patients with acute HSP were diagnosed and observed. The levels of T lymphocyte subsets, natural killer cells (NK cells), and B cells were analyzed by flow cytometry. The serum immunoglobulin G (IgG), immunoglobulin M (IgM), immunoglobulin A (IgA), and complement C3 (C₃) and complement C4 (C₄) levels were detected by velocity scatter turbidimetry.

Compared with the healthy groups, the levels of cluster of differentiation 3 (CD₃), cluster of differentiation 4 (CD₄), B cells, and NK cells and ratio of CD₄/CD₈ in patients with HSP were decreased (P < 0.05). The levels of IgG, IgA, IgM, and C₃ were increased (P < 0.05). Compared with the Kawasaki disease (KD) group, the levels of CD₃, CD₄, CD₈, B cells, NK cells, and IgA in patients with HSP were increased (P < 0.05), and the ratio of CD₄/CD₈ and levels of IgM, C₃, and C₄ was decreased (P < 0.05). Compared with the pneumonia group, the levels of CD₃, CD₄, B cells, and IgA in patients with HSP were increased (P < 0.05), and the ratio of CD₄/CD₈ and levels of IgM and C₄ was decreased (P < 0.05).

Cellular immunity and humoral immunity were all involved in the pathogenesis of HSP. The decline of NK cells, B lymphocyte cells, CD₃, CD₄ the increased secretion of immunoglobulin, and the abnormal appearance of IgA and C₃ may exist during the progression. It may indicate a worse prognosis and increasing the risk of dedifferentiation. Cellular immunity was lower, which lead to increased production of inflammatory mediators and increased secretion of immunoglobulin, which then mediated systemic small-vessel vasculitis. Key Points • The pathogenesis of Henoch-Schönlein purpura (HSP) was not completely illuminated. • There was a lack of disease-specific laboratory abnormalities that can be used in the clinical diagnosis of HSP. • We compared the laboratory abnormalities in the immune system of HSP with KD and pneumonia. • Cellular immunity and humoral immunity were all involved in the pathogenesis of HSP. Cellular immunity was lower, which lead to the following pathological changes.