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Background Innate lymphoid cell (ILC) dysfunction is involved in numerous immune diseases, but this has not been demonstrated in Henoch-Schonlein purpura (HSP). This study aimed to investigate whether ILC dysfunction or imbalance participate in the pathogenesis of HSP. Methods This was a prospective study in patients with HSP who were hospitalized at the Children’s Hospital of Soochow University from June to December 2019. Age- and sex-matched controls were also enrolled. ILC subsets and lymphocyte subpopulations were determined by flow cytometry. The transmission immune turbidimetric method also facilitated the exploration of correlations between ILC subset frequency and lymphocyte subpopulation, as well as serum IgA in HSP patients. Results Fifty-one patients with HSP and 22 control patients were included. There were no differences in age and sex between the two groups. Compared with controls, patients with HSP had higher ILCs in relation to lymphocytes ( P  = 0.036), higher ILCs in relation to PBMCs ( P  = 0.026), higher ILC1s ( P  &lt; 0.001), lower ILC3s ( P  &lt; 0.05), and higher ILC1/ILC3 ratio ( P  &lt; 0.001). Sixteen patients underwent routine therapy combined with methylprednisolone for 7–10 days; ILC1s were significantly decreased ( P  &lt; 0.001) and ILC3s were increased ( P  = 0.033), and ILC1/ILC3 was significantly decreased ( P  &lt; 0.001). Compared with the controls, the ratios of ILCs/lymphocytes and ILCs/PBMC were higher in patients in the arthritis and mixed groups (all  P  &lt; 0.05). ILC1 were elevated in the purpura, arthritis, abdominal, and mixed groups ( P  = 0.027,  P  = 0.007,  P  &lt; 0.001, and  P  &lt; 0.001, respectively). ILC1/ILCs were positively correlated with CD3 + CD8 + T lymphocytes ( r  = 0.3701,  P  = 0.0075). The level of IgA did not correlate with ILCs. Conclusions Higher circulating ILC1s and lower circulating ILC3s appear to be involved in the pathogenesis of HSP.

Increased circulating innate lymphoid cell (ILC)1 and decreased circulating ILC3 are involved in the pathogenesis of Henoch-Schonlein purpura