Serum-migration-inhibitory activity in children with acute infectious mononucleosis.
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Biomedical subjects
Publications and source records attributed to A Bertotto.
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Using an unidirectional leucocyte migration-inhibition (LMI) assay, we investigated the migration-inhibitory activity (LIF) in the sera of 25 infants who developed bronchiolitis following respiratory syncytial virus (RSV) infection. Blood samples for serum-LIF activity detection were obtained from patients the day after admission and two weeks later. The LMI assay revealed serum-LIF activity in 17 (68%) blood samples taken during the acute phase of the disease. In contrast, no inhibition was found in the convalescent blood samples with the exception of 5 (20%). This difference was statistically significant (chi2 = 9.82; P less than 0.005). As positive serum-LIF test is a good in vitro correlate of cell-mediated immunity, our results suggest that cell-mediated hypersensitivity reactions occur during the clinical course of RSV bronchiolitis. These findings are consistent with the hypothesis that alterations of RSV-specific cell-mediated immune mechanisms may be involved in the pathogenesis of this illness.
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Semiquantitative estimates of circulating endotoxin were performed by the limulus test in patients suffering from typhoid fever and other salmonelloses. The test was positive in a large number of cases. However, no clearcut correlation was found between existence of endotoxemia, as such, and pyrexia. A correlation with recent bacteremia was found for highest levels of endotoxin activity. In minor salmonelloses a striking prevalence of positive cases was observed in the age group under one year. These findings were discussed in relation to the diagnostic and pathogenetic facets of the problem.
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CD3+/CD30+ circulating T lymphocytes were found to be increased in the blood of individuals with Down's syndrome (DS; trisomy 21). This finding appears to be related to age as the numbers of CD3+/CD30+ T cells were dramatically enhanced in the circulation of older DS subjects. Since CD30 antigen expression is considered to be a marker of T-helper-2 (Th-2) activation, and Th-2+ cells are associated with certain human pathologies, our data may in some way explain the enhanced susceptibility of DS patients to infections, malignant diseases and autoimmunity.
Forty-six anergic patients (37 males and 9 females, age range 55-79 yr) were selected from ninety-one patients suffering from COPD due to frequent exacerbations and impaired delayed cutaneous reactivity (43.9%). The phenotype of circulating lymphocytes, their proliferative response to a panel of polyclonal T-cell activators and the candidacidal activity (CA) of circulating PMNs (polymorphonuclear cells) were measured. In 13 patients presenting a defective CA of circulating PMNs, the in vitro response of alveolar macrophage CA to r-IFN-gamma was also determined. We found: 1) a significant reduction in the CL response to PHA in COPD patients vs controls; 2) a low PMN-CA in 23 (57%) COPD patients; 3) a non-significant difference in phenotype analysis in patients and controls; 4) lower CA of AMs in COPD patients than in controls; 5) restoration in vitro of CA by r-IFN-gamma in the group of anergic COPD patients presenting depressed CA. We conclude that a defective cell-mediated immunity could be the basis of the enhanced susceptibility to infectious exacerbations in many COPD patients and that, in vitro, it could be reversed by r-IFN-gamma treatment.
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Recent studies in our laboratory have demonstrated that the great majority of human colostral T cells display the phenotypic and functional characteristics of memory T lymphocytes, e.g. were able to proliferate in response to anti-CD3 and anti-CD2 monoclonal antibodies, and to a lesser extent, to the lectin mitogen phytohaemagglutinin. In addition, their production of interferon-gamma after anti-CD3 and anti-CD2 stimuli was similar to that calculated in autologous blood lymphocyte cultures. More interestingly, the proportion of T lymphocytes bearing the gamma/delta T-cell receptor was found to be significantly higher in the mammary secretion than in autologous and heterologous blood samples. Furthermore, these cells were mostly delta-TCS-1+, thereby suggesting that they are actively motile cells capable of migrating from lymphoid to extra-lymphoid body tissues. The fact that the phenotypic pattern of colostral gamma/delta T cells is similar, if not identical, to that of the intestinal intraepithelial counterpart suggests that these cells might originate in the gut-associated lymphoid system and home selectively to the mammary gland late in pregnancy and throughout lactation. However, additional studies are needed to confirm whether milk T lymphocytes are actively involved in the adoptive lactation transmission of cellular immunity to the suckling infant.
Because T-cell dysfunctions have been reported in patients with primary Sjögren's syndrome (SS), peripheral blood mononuclear cell (PBMC) proliferation obtained with anti-CD3 and anti-CD2 monoclonal antibodies was evaluated in these patients. Anti-CD3-induced mitogenesis, which varied widely among the patients, was lower in subjects with evidence of anti-SSA and anti-SSB antibodies than in controls. Moreover, the anti-CD2-induced response was depressed in about half the patients and the nonresponders were mainly those with anti-SSA and anti-SSB antibodies. Phorbol myristate acetate, a protein kinase C activator, used alone or added to anti-CD3, induced greater proliferation in patients than in control PBMC. In contrast, exogenous recombinant interleukin 2 (rIL-2) did not significantly enhance the anti-CD2-induced response of patients' PBMC, as it did in normal PBMC. Peripheral blood and parotid T cells from a patient with well-defined primary SS and parotid enlargement also responded poorly to anti-CD2 stimulation. Exogenous rIL-2 restored T-cell proliferation only in the salivary gland cultures of this patient. The present findings suggest that there is a T-cell activation defect in subjects with primary SS, particularly in those with circulating anti-SSA and anti-SSB antibodies. In addition, the difference in the response to IL-2 of peripheral blood and parotid-infiltrating T cells would seem to indicate that T-cell subsets are differently distributed in the blood and inflammation site.
A case of a 63-year old man, who developed systemic lupus erythematosus three years after an initial diagnosis of small-cleaved centrofollicular lymphoma is described. The diagnosis of SLE was made on the basis of the accepted "1982 revised criteria for the classification of SLE". The autoimmune disease arose after a cycle of total body irradiation, despite the treatment with combination chemotherapeutic doses such a CVP or COAP or Cyclophosphamide, Vincristine, VM-26 and Prednisone. Genetic, immunological and exogenous environmental factors may co-exist and might equally be implicated in the pathogenesis of SLE and malignant lymphoma. However, the onset of SLE after total body irradiation could have been caused by the inactivation of suppressor T lymphocytes, which are known to be sensitive to radiations in vitro.