[Erythroblastometric research on the bone marrow of irradiated subjects].
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Bone Marrow↗
Biomedical subjects
C Fiocchi
Publications and source records attributed to C Fiocchi.
Selective resistance of mucosal T-cell activation to immunosuppression in Crohn's disease.
BACKGROUND & AIMS: The inappropriately high state of T-cell activation found in Crohn's disease could be due to failure to respond to inhibitory signals. We tested the hypothesis that Crohn's disease mucosal T-cells are resistant to the immunosuppressive action of interleukin4. PATIENTS: Patients with Crohn's disease, ulcerative colitis, and other malignant and non-malignant conditions undergoing bowel resection. METHODS: The effect of interleukin-4 on lamina propria mononuclear cells from Crohn's disease, ulcerative colitis and control mucosa was assessed on various T-cell functions: interleukin-2-induced cytotoxicity, soluble interleukin-2 receptor and interleukin-2 production, and expression of mRNA for interleukin-2R and interferon-gamma. RESULTS: Cytotoxicity of control and ulcerative colitis cells was markedly decreased by interleukin-4, whereas Crohn's disease cells failed to be inhibited. Addition of interleukin-4 to interleukin-2-stimulated cultures decreased soluble interleukin-2R production significantly less in Crohn's disease and ulcerative colitis than control cells. In the same cultures, residual levels of interleukin-2 were significantly increased in control and ulcerative colitis, but not Crohn's disease cultures. Finally, Crohn's disease cells were significantly more resistant to interleukin-4-mediated inhibition of spontaneous and interleukin-2-induced expression of interleukin-2Ralpha and interferon-gamma mRNA compared to control cells. CONCLUSIONS: The effector function, receptor expression and cytokine production of Crohn's disease mucosal T-cells are resistant to interleukin4-mediated inhibition. Failure to respond to down-regulatory signals may contribute to persistent T-cell activation and chronicity of inflammation in Crohn's disease.
Adolescent↗
Lymphokines and the intestinal immune response. Role in inflammatory bowel disease.
The study of production of and response to various soluble mediators by gut-derived mucosal mononuclear cells has contributed significantly to a better understanding of the regulation of the intestinal immune system. So far, a number of factors have been investigated in some detail or in a preliminary fashion: interleukin 1, interleukin 2, interleukin 4, interferon gamma and colony-stimulatory factors. Their level of activity, and their effect on the intestinal mucosal immune system are discussed, particularly in regard to their potential role in the pathogenesis of inflammatory bowel disease.
Humans↗
The immune system in inflammatory bowel disease.
During the last few decades it has become increasingly evident that inflammatory bowel disease (IBD) is associated with abnormalities of systemic and mucosal immunity. This association has slowly moved from the phenomenological to the mechanistic level, and today there is solid evidence that the immune system mediates inflammation and tissue damage in the gut of patients suffering from IBD. However, the exact mechanisms of injury and what triggers such mechanisms are yet to be understood in spite of expanding knowledge of the cellular and molecular events underlying gut inflammation. Phenomena detected in the peripheral blood of IBD patients reflect some, but not all, of the events occurring in the gut and have limited meaning. On the contrary, the investigation of phenomena occurring in the inflamed mucosa has yielded valuable information on which progress in the understanding of IBD pathogenesis and the development of new therapies are currently based. It seems that all immune and non-immune components of the mucosa are involved in IBD, either directly or indirectly, as shown by abnormalities of humoral and cell-mediated immunity, cytokine and growth factor, eicosanoids, neuropeptides, reactive oxygen and nitrogen metabolises, cell adhesion molecules, apoptosis, and non-immune cells. Because of the multiplicity and complexity of the interactions of all these elements it is presently impossible to discern between primary and secondary, and pathogenic and non-pathogenic phenomena. In spite of these difficulties, an impressive amount of information is being gathered which is translated, at times in a preliminary or empirical fashion, into novel immunopathology-based forms of treatment.
Autoimmunity↗