Interleukin-35 promotes the differentiation of regulatory T cells and suppresses Th2 response in IgG4-related type 1 autoimmune pancreatitis

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  • Interleukin-35はIgG4関連1型自己免疫性膵炎の制御性T細胞の分化を誘導し，Th2免疫応答を抑制する
  • Interleukin-35 ワ IgG4 カンレン 1ガタ ジコ メンエキセイスイエン ノ セイギョセイ Tサイボウ ノ ブンカ オ ユウドウ シ,Th2 メンエキ オウトウ オ ヨクセイ スル

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Abstract

<p>Type 1 autoimmune pancreatitis (AIP) is an intractable disease involving immune disorders. AIP has Th2-type immune response abnormalities, but the pathophysiology has not yet been elucidated. It has been reported that the pathophysiology of AIP involves abnormalities in regulatory T cells (Tregs) and changes in the proportions of naïve Tregs (nTregs) and activated effector Tregs (eTregs). Interleukin 35 (IL-35) is a newly discovered inhibitory cytokine, which is mainly produced by Tregs. We analyzed the association of Tregs and IL-35 in AIP. As a result, plasma IL-35 was high in AIP. The ratios of nTregs/CD4 positive cells and eTregs/CD4 positive cells in the peripheral blood of AIP patients were low and high, respectively. However, the gene expression of EBi3 and IL-12p35 in nTregs and eTregs did not increase. In pancreatic tissues, AIP had a large number of EBi3 or IL-12p35 positive cells, and also a large number of EBI3 and IL-12p35 double-positive cells. These findings suggest that IL-35 contributes to the immune-pathological conditions of AIP through the suppression of Th2 responses and promotion of the differentiation of Tregs. </p>

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