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M Frisoni

Publications and source records attributed to M Frisoni.

29 records · Page 2Linked to original sources
PubMed1986

Gluten specific suppressor T cell dysfunction in coeliac disease.

A T lymphocyte direct migration inhibition factor test has been used to investigate the function of the specific suppressor T cell population controlling the immune response to gluten in coeliac disease. The test has been carried out in 21 adult coeliac patients, 22 Mantoux- healthy controls and eight Mantoux+ donors using gluten fraction III and purified protein derivative, as antigens. All coeliacs, but two, were Mantoux-. When gluten fraction III was used a significant migration inhibition was observed in coeliac patients compared to controls; such migration inhibition was abrogated by coculturing in a 1:1 ratio coeliac T cells with T cells from controls or Mantoux+ donors. On the contrary, the addition to coeliac T cells of T lymphocytes from other coeliacs did not abolish migration inhibition to gluten. Pretreatment of normal T cells with mitomycin C prevented their abrogating activity on migration inhibition of coeliac T lymphocytes. When purified protein derivative was used as antigen a significant migration inhibition was observed in Mantoux+ donors compared with healthy subjects and such migration inhibition was abolished by co-culturing T cells from Mantoux+ donors with those from Mantoux- controls and coeliac patients. Our results show that coeliac T cells, while retaining their ability to suppress the immune response to purified protein derivative, cannot suppress the immune response to gluten and are consistent with the hypothesis that a gluten specific suppressor T cell dysfunction, rather than a generalised T lymphocyte defect, may play a role in the pathogenesis of coeliac disease.

Adult↗
PubMed1985

DR and non-DR Ia allotypes are associated with susceptibility to coeliac disease.

We have studied the frequency of HLA-DR, -MT, and -MB antigens in adult patients with coeliac disease and in a group of healthy controls, evaluating the strength of the observed associations by measuring the aetiologic fractions. Among the antigens significantly associated with coeliac disease, MB2 (DQw2) showed an aetiologic fraction higher than those of DR3 and DR7. Our results suggest that MB2, as associated more frequently than other specificities with a hypothetical disease predisposing gene, may play a role in the pathogenesis of coeliac disease. The significant association of DR3 and DR7 with coeliac disease may be ascribed to linkage disequilibrium of these antigens with MB2.

Adolescent↗
PubMed1985

Specificity of leucocyte migration inhibition test in coeliac disease. A reassessment using different gluten subfractions.

Production of leucocyte migration inhibition factor by peripheral blood leucocytes in response to challenge with gluten fractions has been proposed as a reliable in vitro test for the diagnosis of coeliac disease. We have performed the leucocyte migration inhibition test with two different gluten fractions, GFIII and B2, in untreated and treated coeliac patients, patients with other intestinal diseases (abnormal controls) and healthy controls, and evaluated the sensitivity, specificity and positive and negative predictability of the test for the diagnosis of coeliac disease. Using GFIII as antigen leucocyte migration was significantly inhibited, compared to healthy controls, not only in treated and untreated coeliacs but also in abnormal controls. Using B2 gluten subfraction as antigen only treated coeliacs and abnormal controls differed significantly from healthy controls. The elevated number of abnormal controls showing migration inhibition consistently affected the diagnostic value of the test, which did not vary using B2 subfraction instead of GFIII as antigen. Our study confirms previous observations of gluten sensitization, as detected by leucocyte migration inhibition, in coeliac patients but strongly questions the claim that coeliac disease can be diagnosed on the basis of a positive leucocyte migration inhibition test without the need for intestinal biopsy.

Adolescent↗
PubMed1984

Return of splenic function after splenectomy: how much tissue is needed?

Ninety patients whose spleen had been removed either because of trauma (41 cases) or as an elective procedure (49) were investigated for return of splenic function by counting pitted red cells and examining spleen scans made after injection of heat damaged 99mTc labelled red cells. There was no significant difference in the proportion of pitted red cells between the two groups of patients. Evidence of splenic tissue in scintiscans was not invariably associated with low pitted red cell values, suggesting that the presence of splenic tissue did not necessarily mean return of splenic function. In every patient whose proportion of pitted red cells was less than 16.2% the scintiscan showed splenic uptake. The proportion of patients with pitted red cell values below 16.2% was significantly higher in the group operated on for trauma, and it is concluded that this was due to splenosis. A high inverse correlation between pitted red cell counts and computed splenic volumes was found. Patients with pitted red cell values of less than 16.2% had computed volumes of 22-133 cm3; below this range the proportion of pitted red cells rose very sharply. These results confirm that splenosis occurs in adults, though less often than in children, and suggest that when splenic tissue is to be implanted a graft of at least 20-30 cm3 is needed to ensure satisfactory return of splenic function.

Adolescent↗
PubMed1983

T-lymphocyte subsets in adult coeliac disease.

1. As a defect of suppressor function has been hypothesized in the pathogenesis of coeliac disease, we measured, by monoclonal antibodies, the inducer/suppressor T-cell ratio in adult coeliac disease. 2. No statistical difference was observed between coeliac patients and healthy controls, irrespective of treatment and HLA status. 3. These results do not show an imbalance in the inducer/suppressor T-cell ratio in coeliac disease.

Adult↗
PubMed1983

Effect of gluten-free diet on splenic hypofunction of adult coeliac disease.

Splenic function has been serially measured by counting pitted red cells in 15 coeliac patients, before and during a gluten-free diet. The basal percentage values of pitted cells decreased significantly during treatment but no correlation was observed between the duration of the gluten-free diet and the percentage of recovery of splenic function over basal values. Out of six coeliacs with pitted cell values consistent with splenic hypofunction, three showed a total recovery after gluten withdrawal. Our data suggest that, contrary to recent reports, hyposplenism in adult coeliac disease is improved by a gluten-free diet, and that environmental factors may be important in determining and maintaining this complication.

Adult↗
PubMed1982

Splenic function in childhood coeliac disease.

We measured splenic function using a simple, non-isotopic method in childhood coeliac disease. No patients were shown to have hyposplenism. This has important clinical and therapeutic implications.

Adolescent↗