ArticleClinical and experimental immunology2003
TGF-beta1 production in inflammatory bowel disease: differing production patterns in Crohn's disease and ulcerative colitis.
Article in Clinical and experimental immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 104 citations in OpenAlex.
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Corrections and comments
- Erratum issued
Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-beta (TGF-beta) is an inhibitory cytokine recognized as a key regulator of immunological homeostasis and inflammatory responses. TGF-beta is involved in experimental models of oral tolerance and in the pathogenesis of experimental colitis. Patients with inflammatory bowel disease (IBD) have inappropriate T cell responses to antigenic components of their own intestinal microflora, suggesting the presence of a disorder in the normal mucosal immune mechanism that ensures the down-regulation of responses to harmless constituents in the microflora. To evaluate the contribution of TGF-beta to this imbalance, we measured TGF-beta1 production by lamina propria mononuclear cells (LPMC) and T cells isolated from tissue specimens of patients with Crohn's disease (CD), ulcerative colitis (UC) and controls. Cells were cultured in the presence or absence of anti-CD2 plus anti-CD28 MoAbs and TGF-beta1 production in culture supernatants was measured by ELISA. LPMC isolated from CD patients produced significantly less TGF-beta1 than controls when stimulated via CD2 plus CD28 pathways (P = 0.001)] conversely, in UC patients increased production of TGF-beta1 compared to controls was observed (P = 0.0005). These differences were also observed with purified lamina propria (LP) T cells in both diseases and were associated with the presence of inflammation. Thus, TGF-beta1 production shows contrasting secretion in CD and in UC, probably as a consequence of the different Th polarization. The absolute or relative defect in TGF-beta1 production observed in CD and UC may contribute to the perpetuation of inflammation.
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