Signaling Molecule IL-38 Can Reduce Inflammation, May Be Therapy Target, Study Finds
Signaling Molecule IL-38 Can Reduce Inflammation, May Be Therapy Target, Study Finds
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Signaling Molecule IL-38 Can Reduce Inflammation, May Be Therapy Target, Study Finds
Signaling Molecule IL-38 Can Reduce Inflammation, May Be Therapy Target, Study Finds
https://www.sciencedirect.com/science/article/pii/S016158902030482X?via%3Dihub
https://www.ncbi.nlm.nih.gov/pubmed/32950755?dopt=Abstract
TITLE:
Blockade of Th17 response by IL-38 in primary Sjögren’s syndrome.
DESCRIPTION:
Blockade of Th17 response by IL-38 in primary Sjögren’s syndrome.
Mol Immunol. 2020 Sep 17;127:107-111
Authors: Luo D, Chen Y, Zhou N, Li T, Wang H
Abstract
BACKGROUND: T helper 17 (Th17) cell responses were involved in the pathophysiology of primary Sjögren’s syndrome (pSS). IL-38 has been reported to inhibit the secretion of chemokines involved in Th17 pathway. This study aimed to explore the regulation of Th17 response by IL-38 in pSS.
METHODS: Twenty-four pSS patients, 15 non-pSS control, and 13 health subjects were recruited. The expression of IL-38 and Th17 cytokines were detected and compared between pSS and controls. Human peripheral blood mononuclear cells (PBMCs) and minor salivary gland mononuclear cells (MSGMs) were purified and stimulated by IL-38. The differentiation and function of Th17 cells were evaluated by PCR and enzyme-linked immunosorbent assay (ELISA).
RESULTS: The pSS patients presented with significantly lower expression of IL-38 and higher Th17 cytokines (IL-17 and IL-23) compared with both non-pSS and healthy controls. The IL-38 inhibited the differentiation and function of Th17 responses from PBMCs and MSGMs. The IL-38 treatment could inhibit the Th17 response in mice model.
CONCLUSIONS: IL-38 inhibits T helper 17 type responses in pSS, suggesting that IL-38 may be used as potential treatment target in pSS.
PMID: 32950755 [PubMed – as supplied by publisher]
PMID:
PubMed:32950755
DATE FOUND:
09/21/20 06:01AM
LINK / URL:
https://www.ncbi.nlm.nih.gov/pubmed/32950755?dopt=Abstract