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Lymphocytes bearing the T cell receptor gamma delta (TCR-gamma delta) were searched for in human early milk lymphocyte suspensions by two colour cytofluorimetric analysis. It was found that the proportion of TCR-gamma delta+ cells was twofold greater in colostrum than in either autologous or heterologous blood samples. Additional studies are needed to determine whether this particular subset of lymphocytes is involved in the lactation transmission of cellular immunity.

Naive (unsensitized) and memory (antigen-primed) T cells can be phenotypically distinguished on the basis of the high or low intensity with which they express a number of immunologically relevant lymphocyte membrane antigens, including CD45R, CDw29, UCHL1, LFA-1, LFA-3, CD2 and Pgp-1. Here we report that in contrast to the two major T cell subsets found in the blood, milk T lymphocytes are almost exclusively composed of the one which exhibits the CD45Rlow, CDw29, UCHL1, LFA-1high memory T cell phenotype. In addition, while milk and autologous blood cells expressed similar levels of CD3 surface antigens, CD2 and ICAM-1 expression was approximately twofold greater on the milk T lymphocytes. This agrees with the finding that whereas colostrum T cells respond poorly to PHA, they proliferate and produce interferon-gamma normally when stimulated with either the anti-CD3 or anti-CD2 monoclonal antibodies. The selective colonization of the mammary gland during lactation by a population of T lymphocytes which displays the phenotype and functional characteristics of memory T cells may be one of the mechanisms whereby the suckling infant benefits form its mother's immunological experience.

The aim of this paper was to evaluate the efficacy of treatment with heparin in children with bronchiolitis. We studied 30 children (average age 11.3 months) with bronchiolitis; 15 subjects were submitted to a supportive therapy with an adjunct of sodium heparin (50 U/Kg/24 h i.v.) for a time lasting 24-36 hours. The control group was managed with supportive therapy only. We considered the days of the disease and the persistence of symptoms since the admission as peculiar parameters between the two groups. The results appeared to be highly significant in the heparin treated group, with a mean duration of the diseases of 3.06 days compared to 5.53 days of the controls (p less than 0.001). These data are supportive for a possible utilization of the heparin in bronchiolitis but much more experiments are needed to confirm these results.

From observations in the Republic of Argentina it is concluded that the regular intake of drinking water containing more than 0.1 ppm of arsenic leads to clearly recognizable signs of intoxication and ultimately in some cases to skin cancer.

Viral infections are often associated with immunodeficiency states. Although T lymphocytes have been thought to suppress the host's immune response, the precise cellular basis for this phenomenon remains unclear. Therefore, we characterized peripheral blood mononuclear cells from 9 measles virus-infected children by means of monoclonal antibodies directed against surface antigens expressed on human T lymphocytes and T-cell subsets. In addition, the measles lymphocyte blast transformation response to the T-cell mitogen phytohaemagglutinin (PHA) was evaluated as an index of specific T-cell immunocompetence. During the course of measles, there was a slight reduction in the proportion of total circulating T cells, with a relative decrease in helper-inducer and a parallel increase in suppressor-cytotoxic T lymphocytes. The PHA lymphocyte blastogenic response was found to be defective in children with measles and, interestingly, there was a significant negative correlation between the reduced PHA blast transformation value and the increased proportion of suppressor-cytotoxic cells. The biological implications of these finding with respect to the underlying immunopathology of the measles virus infection are discussed.

An indirect immunofluorescence staining technique was employed to evaluate the TQ1 and 5/9 monoclonal antibody lymphocyte reactivity in 10 cord blood mononuclear cell (MC) preparations enriched of E-rosette-forming cells (E+). Ten adult E+ MC populations were used as controls. Unfractionated T4+ cord and adult MC positively selected by panning procedure were also assayed. The results of these experiments, taken together, suggest that there is an overexpanded neonatal T cell subset which displays a previously unrecognized immunophenotype (T4+, TQ1+, 5/9+). Whether these lymphocytes are involved in the wellknown fetal-maternal immunosuppressive mechanisms of whether they are a further example of neonatal phenotypic immaturity remains to be elucidated.

Since infectious mononucleosis (IM) mononuclear cells spontaneously release the leukocyte (migration) inhibitory factor (LIF) in culture and since previous experiments in our laboratory have demonstrated that one or more substances with LIF-like activity are detectable in the serum (serum LIF) of young patients with heterophile-positive IM, an investigation was carried out to determine both the in vitro and in vivo LIF production in a series of IM patients sampled during the acute phase of the infection. The observation than only the unstimulated lymphocytes from serum LIF-positive IM patients released LIF in culture suggests that a single active product is involved in the in vitro and in vivo LIF activities observed in Epstein-Barr virus (EBV) infected subjects. The biological implications of this finding with respect to the underlying immunopathology of the EBV IM syndrome are discussed.

Previous experiments in our laboratory have demonstrated that circulating endogenous leucocyte (migration) inhibitory factor (serum LIF), or a lymphokine with LIF-like activity, may be involved in the impaired cellular immune response observed during the acute phase of the Epstein-Barr virus (EBV) induced infectious mononucleosis (IM). To determine whether serum LIF activity is associated with immunoregulatory IM T-cell subset abnormalities, we analyzed the peripheral blood T-cell populations in a series of acute serum LIF-positive and LIF-negative IM patients by means of T-lymphocyte-specific monoclonal antibodies. Although there was both activation and increase of suppressor/cytotoxic T cells in all IM patients sampled in the acute stage, the relative and absolute numbers of suppressor lymphocytes were found to be significantly higher in those who had LIF activity in their serum. It is postulated that EBV infection can preferentially activate a specific T-cell subpopulation which, in its turn, inhibits the overall host immune response, possibly by a LIF-induced feedback suppression mechanism.

The lymphocyte surface phenotypes in the blood of 7 non-institutionalized adults with trisomy-21, and in 10 karyotypically normal control subjects, were analysed by fluorescent microscopy with an OKT series of monoclonal antibodies. Whereas the proportions of OKT3+, OKT4+ and OKT6+ cells were similar in the two groups, the percentages of both OKT8+ and OKT10+ trisomic lymphocytes were significantly higher. The biological implications of these findings with respect to the underlying immunopathology of Down's syndrome are discussed.

Peripheral blood mononuclear cells from 10 subjects with cytogenetically documented Down's syndrome (DS) and from 10 age- and sex-matched healthy controls were assayed for their ability to proliferate in response to phytohaemagglutinin, anti-CD3 (OKT3), or anti-CD2 (T11(2) plus T11(3] monoclonal antibodies. Interleukin 2 (IL-2) receptor expression and IL-2 production in mitogen-pulsed lymphocyte cultures was also investigated in parallel. DS cells responded poorly to all the blastogenic stimuli used in this study. Under certain experimental conditions (anti-CD3 or anti-CD2 antibody stimulation), the patients' lymphocytes expressed low levels of IL-2 surface receptors and failed to produce normal amounts of this lymphokine. Studies are currently in progress in our laboratories to determine whether these defects are due to an impairment of the early signalling events surrounding the complexing of CD3, CD2, or lectin receptors to their respective ligands.

During the intestinal phase of hepatobiliary imaging studies in four patients, unusual small intestinal abnormalities were noted. These findings were correlated with surgery in three patients. Recognition of these patterns gives additional clinical information of significant diagnostic value. Further attention to small intestinal pattern and/or radionuclide evaluation of small intestine is a promising method of noninvasive evaluation of clinically suspected small intestinal infarction and obstruction.

The non-specific mitogen phytohaemagglutinin (PHA) and an anti-CD3 (OKT3) monoclonal antibody were used to measure the lymphocyte proliferative response in blood samples from 15 subjects with Down's syndrome. Blood from 15 healthy controls closely matched for age and sex was also assayed. The mean blastogenic value in PHA stimulated patient lymphocyte cultures was similar to that calculated in the controls. In contrast, the mitogenic response of lymphocytes from patients with Down's syndrome to anti-CD3 stimulation was on average significantly reduced. Immunofluorescence studies and additional experiments carried out by using semiallogeneic (maternal) monocytes as a source of antigen presenting cells showed that the impaired anti-CD3 induced mitogenesis in Down's syndrome could not be ascribed either to a lack of binding of the antibody to the trisomic cells, or to a defective monocyte-T cell interaction. These findings help to explain the cellular basis of the immune defect in Down's syndrome.

A patient described as a 45,X male (Forabosco et al. 1977) was examined for the presence of Y-specific DNA by using various probes detecting restriction fragments from different regions of the Y chromosome. Positive hybridization signals were obtained for Yp fragments only. In situ hybridization with two different probes, pDP31 and the pseudoautosomal probe 113F, led to a clear assignment of the Yp sequences to the short arm of one chromosome 18. Cytogenetically, the presence of all of Yp including the Y centromere on 18p could be demonstrated replacing a segment of similar size of 18p. Thus, the Y/18 translocation chromosome is dicentric structurally, but it was shown to be monocentric functionally with the no. 18 centromere active. Gene dosage studies with the probe B74 defining a sequence at 18p11.3 demonstrated a single dose of this sequence in the patient. In agreement with these observations, the patient shows clinical signs of the 18p-syndrome. It is concluded that in XO males in general, the X is of maternal origin while the maleness is due to a de novo Y/autosome translocation derived from the father. Depending on the nature of the autosomal deficiency caused by the Y/autosome translocation, the patient may have congenital malformations.

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.

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.

A relative decrease in helper and a parallel increase in suppressor-cytotoxic T lymphocytes was found in the blood of six habitually aborting women, as compared with the T-cell subset distribution in ten normal multiparae and eight multigravid post-partum women. It is suggested that an imbalance between the immunoregulatory T-cell subpopulations may contribute to the rejection of the semiallogenic fetus.

The distribution of T-lymphocyte subsets in human early milk was determined by immunofluorescence analysis of reactivity with monoclonal antibodies of the OKT series. A novel finding was that the T-lymphocyte population in human milk contains both OKT4 (helper/inducer phenotype) and OKT8 (suppressor/cytotoxic phenotype)-positive subsets. The relative ratio of OKT4 to OKT8-positive T-cell subsets in milk, however, was generally higher than that observed for peripheral blood T cells.

Leucocyte migration-inhibitory activity was found in the sera (cord blood) of 15/28 (53%) healthy, fullterm newborn infants as opposed to only 3/28 (10,7%) control children under three years of age (P less than 0,005). It is postulated that the migration-inhibitory activity may be related to lymphokine-dependent mechanisms.

The proliferative response of purified T cells to anti-CD2 monoclonal antibodies (T112 plus T113) was found to be markedly reduced in 12 subjects with Down's syndrome (DS). The addition of phorbol ester PMA, which activates Ca2+/phospholipid-dependent enzyme protein kinase C, or calcium ionophore A23187, which increases intracytosolic free Ca2+ concentration, enhanced, but did not normalize, the defective anti-CD2-mediated T-cell mitogenesis. In contrast, the proliferation of resting lymphocytes from trisomic patients was comparable to that of the control cells when PMA and A23187 were used as co-blastogenic reagents. Because PMA and A23187 together bypass the early activation pathways and promote T-cell growth through the direct induction of membrane interleukin 2 (IL-2) receptor expression and IL-2 synthesis and secretion, it could reasonably be hypothesized that the faulty DS T-cell activation induced by antigen or mitogen is due to a deranged transmembrane signal transduction, rather than a defect in the later intracellular events.

We studied 500 cases of head injury in children from 0 to 12 years of age, to investigate the relationship between clinical signs and symptoms and the results Rx, EEG, F.O. and TAC.