ArticleClinical and experimental immunology2025
Role of a new truncated CD74 isoform in increased IL-17 secretion from stromal-immune cell interactions.
Article in Clinical and experimental immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionStromal-immune cell interactions promote pro-inflammatory cytokine secretion such as IL-17. IL-17 is involved in several chronic inflammatory diseases, affecting joints and skin. Podoplanin has been already identified as partially involved in high IL-17 secretion resulting from these cell interactions.
methodsThe aim of this study was to identify new molecules, using co-cultures of activated peripheral blood mononuclear cells and synoviocytes (5:1 ratio). Cell interactions were critical to induce a high IL-17 production. The blockade of podoplanin inhibited this production, approximately 40%, confirming the contribution of other molecules. A battery of mouse monoclonal anti-human RA synoviocyte antibodies were tested in co-cultures and several were selected for their inhibitory effect on IL-17.
resultsCloning by expression allowed identifying the target of the selected 8350 antibody, a truncated isoform of CD74. CD74 blockade in co-cultures by 8350 antibody and a commercial antibody inhibited IL-17 production by 40%, but 8350 antibody had a limited effect on IL-10 inhibition. Furthermore, cell interactions increased CD74 expression, at mRNA and protein levels.
conclusionThis study identified truncated CD74 isoform as a novel molecule directly involved in high IL-17 secretion resulting from cell interactions. Inhibition of this truncated CD74 could represent a new therapeutic option for diseases with IL-17 involvement.
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