TGF-β1 production in inflammatory bowel disease: differing production patterns in Crohn's disease and ulcerative colitis
Autor: | G. Mumolo, Roberto Tersigni, B. Del Zotto, Chiara Montesani, Monica Boirivant, Annamaria Pronio |
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Jazyk: | angličtina |
Rok vydání: | 2003 |
Předmět: |
Adult
medicine.medical_specialty medicine.medical_treatment T cell T-Lymphocytes Immunology Inflammatory bowel disease anergy Statistics Nonparametric Immune tolerance Interferon-gamma Crohn Disease Transforming Growth Factor beta Internal medicine Clinical Studies medicine Immunology and Allergy Humans human Colitis mucosa Cells Cultured Aged Crohn's disease Lamina propria tolerance business.industry cytokines inflammation suppression Middle Aged medicine.disease Ulcerative colitis Endocrinology Cytokine medicine.anatomical_structure Leukocytes Mononuclear Colitis Ulcerative Interleukin-5 business |
Popis: | SUMMARY Transforming growth factor-β (TGF-β) is an inhibitory cytokine recognized as a key regulator of immunological homeostasis and inflammatory responses. TGF-β 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-β to this imbalance, we measured TGF-β1 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-β1 production in culture supernatants was measured by ELISA. LPMC isolated from CD patients produced significantly less TGF-β1 than controls when stimulated via CD2 plus CD28 pathways (P = 0·001)] conversely, in UC patients increased production of TGF-β1 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-β1 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-β1 production observed in CD and UC may contribute to the perpetuation of inflammation. |
Databáze: | OpenAIRE |
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