Stress, cortisol concentrations, and lymphocyte subpopulations.
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Biomedical subjects
Publications and source records attributed to N A Byrom.
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During episodes of acute anterior uveitis, patients had a T-lymphopenia and a temporary increase in B-lymphocytes. The T-lymphopenia was not present in patients investigated early in their first attacks, and it persisted after the patients recovered clinically. In household contacts of patients with uveitis, there was a temporary T-lymphopenia. A similar degree of T-lymphopenia was present in patients with ankylosing spondylitis who had not had uveitis, but not in their household contacts. In patients with spondylitis, there was no greater reduction of T-cells when they had episodes of uveitis. In all groups of subjects studied, T-lymphopenia could be abolished, in vitro, with thymosin, a bovine thymic-hormone estract. The finding of T-lymphocyte depletion in the contacts of uveitis patients, as well as in the patients themselves, suggests that there may be lateral transmission of an infective agent (or agents) in the households during (or before) attacks of uveitis.
We have searched the literature for data on the in vitro assessment of immune status in atopic eczema patients, and have found much confusion. The major findings are tabulated. It is concluded that atopic eczema is a form of immune deficiency, although it is unclear whether this is a primary or secondary defect. Most authors find a T-lymphocyte deficit while eosinophils, B lymphocytes and serum IgE are increased. Serum IgE levels appear to correlated with severity of eczema symptoms. We have previously suggested that T-lymphocyte levels are overestimated in eczema when fetal calf serum is used in the E-rosette assay. Analysis of the literature for the effect of this serum in the assay confirms that there is a T-lymphocyte deficit in atopic eczema, but that the serum masks it. Thus, much of the confusion surrounding this issue can be resolved.
Thirty children with atopic eczema were compared with an equal number of age-matched healthy children. The mean peripheral blood T-lymphocyte level was lower in the eczema group (mean 1,197/mm2 as against 1,702/mm3; P = 0 . 003). This difference was abolished in vitro by thymosin, a thymic hormone extract. Positive correlations were found between eczema severity and: eosinophilia; hyperimmunoglobulinaemia E; but not T lymphopaenia. Thymosin-inducible T-cell (Ti) counts correlated with plasma IgE levels, suggesting that these Ti cells may be immature suppressor T cells. If this T-cell deficiency represents inadequate suppression of IgE responses, then a trial of treatment with thymosin appears to be warranted.
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Thirty asthmatic children were compared with an equal number of age-matched healthy children. The mean peripheral blood T-lymphocyte level without foetal calf serum was lower in the asthmatic group (mean 970/mm3, as against 1740/mm3; P less than 0.0001), but this difference was abolished by adding foetal calf serum or thymosin, thus explaining how quite severe T-cell deficiency can be missed by widely used methods. The degree of eosinophilia and the degree of elevation of the plasma IgE level in the asthmatic patients were positively correlated. Positive correlations were also shown between the degree of severity of the asthma, the degree of eosinophilia and the degree of elevation of the plasma IgE level, but not the degree of depression of the T-cell numbers. If this T-cell deficiency reflects an inadequate suppression of IgE responses, a clinical trial of thymosin appears to be warranted.
E rosette-forming (T) lymphocytes and surface immunoglobulin-bearing lymphocytes were estimated in 85 patients with malignant melanoma. The melanoma patient group had lower mean levels of T lymphocytes and higher mean levels of immunoglobulin-bearing (? B) lymphocytes than did normal subjects. The absolute and percentage depressions of T-cell levels in the melanoma patients were stage-related, as was the depression of total lymphocyte and B-lymphocyte levels. The T lymphopenia in the melanoma patients could, in vitro, be partially abolished by fetal calf serum (as used in many E rosetting methods), and could be totally abolished by thymosin fraction 5 (Hoffmann-La Roche) at optimum concentration. In view of the ability of thymosin to restore T cells to normal levels in all of the T-lymphopenic patients, a clinical trial of this hormone in selected melanoma patients of all stages appears to be warranted.
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A new technique is described whereby viable infiltrating cells can be freed from skin biopsy specimens. The specimens are incubated with collagenase and then mechanically disaggregated. The liberated cells are still suitable for immunological and morphological study. Using this method, the nature of the dermal infiltrate in patients with skin reticuloses was compared with that in lichen planus. A predominance of T cells was found in mycosis fungoides, the Sezary syndrome, and lichen planus, and of B cells in non-Hodgkin lymphomas.
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