Imbalance of T helper and T suppressor cells and reduced plaque-forming cell capacity of mononuclear cells from patients with mycosis fungoides.
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Biomedical subjects
Publications and source records attributed to J R Jensen.
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Soluble IgE-binding and IgG-binding factors were generated by 18-hour incubation at 4 degrees C of the human B cell lines RPMI 8866 and Daudi. These cells express Fc receptors for IgE (Fc epsilon R) and IgG (Fc gamma R), respectively. Binding factors specifically inhibited FcR on both lymphocytes and monocytes, and bound to Ig-Sepharose supports. RPMI 8866 cells and Daudi cells were radiolabeled with 125I by the lactoperoxidase method, and the soluble factors were labeled by the chloramine T method. Affinity chromatography of the soluble factors was performed with IgE-Sepharose, IgG-Sepharose and lentil-lectin-Sepharose followed by sodium dodecyl sulphate polyacrylamide gel electrophoresis and autoradiography. The finding of a common 22,000-dalton protein in supernatants with IgE binding, IgG binding, and non-binding activity is discussed in relation to methodological difficulties and the ambiguous results in the literature, as well as the possibility of a complex formation of macromolecules with binding factor activity.
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The natural killer cell cytotoxicity of peripheral blood lymphocytes from twenty-one patients with moderate to severe atopic dermatitis was studied directly by a single cell assay. Suspensions of conjugated effector cells bound to target cells were examined with a light microscope to evaluate the cell lysis using trypan blue exclusion. The binding to the K562 target cells and the kinetics of lysis were normal among the patients' lymphocytes, but the percentage of active natural killer cells in the conjugates and the lymphocyte population was found to be significantly reduced. Our results raise the possibility that the number of active natural killer cells may be reduced and/or modulated by enhancing and suppressing signals in patients with atopic dermatitis.
We have studied the secretion of immunoglobulin in vitro from blood lymphocytes in twenty-one patients with primary or secondary syphilis before and after treatment of their disease. Polyclonal activation of B lymphocytes with pokeweed mitogen is dependent upon T lymphocytes. Using the inversed haemolytic plaque cell assay we found a normal secretion in vitro of immunoglobulin in both primary and secondary syphilis. Our results indicate that patients with syphilis retain a normal immune regulation of B lymphocyte immunoglobulin secretion in vitro.
Three hundred thirty cases were selected from an endodontic practice. Postoperative and recall radiographs of each case were examined by four endodontists for an interpretation of treatment success or failure. One hundred eighteen cases were examined a second time by each endodontist. Initial analysis showed substantial inconsistency in both inter- and intraobserver interpretation. The cases were then categorized by average radiographic density differences within radiograph sets, anatomic location of the treated tooth, technical compatibility within radiograph sets, and by length of time between postoperative and recall radiographs. It appears that these factors do not affect reliability of success/failure interpretation.
The peripheral blood lymphocytes of 36 adult patients with moderate to severe atopic dermatitis had reduced natural killer (NK) cell activity when measured against 51Cr-labeled K 562 cells. The decrease in NK cells activity was not related to the serum IgE level, but was related to the severity of the skin disease. Addition of autologous monocytes of the assay reduced the NK cell activity and concealed the enhancing effect of gamma-interferon addition in a 4-h assay. The NK cell activity of lymphocytes could be reduced in vitro by addition of prostaglandin E1, or increased by addition of gamma-interferon similar to lymphocytes from persons without atopic disease. Our present findings raise the possibility that the reduced NK cell activity may be secondary to the skin disease, and due to in vivo interaction between NK cells and monocytes, or to low numbers of NK cells in peripheral blood.
Eighteen patients with mycosis fungoides were studied in order to establish cell lines that might be associated with the human T cell leukaemia-lymphoma virus (HTLV). Three T cell lines were established, two from affected skin and one from a lymph node showing dermatopathic lymphadenopathy. The T cells expressed OKT3 and OKT4 antigens. They temporarily expressed an HTLV p19-like antigen in up to 5% of the cells during culture. None of our patients had lymphocytosis or abnormal lymphocytes, except one patient with Sézary's syndrome. We could not establish T cell lines from peripheral blood, but five B lymphoblastoid cell lines were obtained, all positive for the Epstein-Barr virus nuclear antigen. Our finding that T cell lines can be established from skin biopsies and lymph nodes of patients with mycosis fungoides, but not from the blood, supports the concept of a malignant T lymphocyte primarily localized in the skin. The temporary expression of HTLV p19 antigen may indicate the presence of retrovirus, but further studies are needed.
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Release of immunoglobulin-binding factors was induced from cultured human lymphoblastoid cells in a serum-free environment by incubation at 37 degrees. RPMI-8866 cells expressing Fc receptors for IgE (Fc epsilon R) and Daudi cells expressing Fc receptors for IgG (Fc gamma R) released IgE- and IgG-binding factors, respectively. The factors induced were shown to have: (i) specificity of rosette inhibition; (ii) specificity of Ig-binding; and (iii) a glycoprotein nature. The IgE-binding factor remained stable, whereas the IgG-binding factor showed a time-dependent degradation and a concurrent change in specificity from IgG- to IgE-binding. The occurrence of this change was paralleled by a disappearance of a 125,000 mol. wt. protein on autoradiograms of SDS-PAGE of the IgG-binding factor preparation. These results raise the possibility that the released IgG-binding factor is found in a polymerized form which may dissociate into subunits in aqueous solution, and that common subunits may exist with regard to IgE- and IgG-binding factors, some of which may either lose their activity, or bind to both IgE and IgG with different affinities.
Fifth-grade students were subjects in a study designed to determine adequacy of dietary intakes and the contribution of the school lunch to diet adequacy. Seven-day food records and 24-hour food recall data showed that only protein and riboflavin were consumed in adequate quantities. There were wide individual variations in consumption of calcium, iron, thiamin, niacin, vitamin A, and ascorbic acid. Vitamin A and ascorbic acid intakes were not significantly related to family income or the mother's education, but fat consumption correlated positively with family income. School lunches as served must provide at least one-third of the RDAs. Meals served in this study contained from 110% to 295% of the nutrients included in the Type A lunch. Even though less than 65% of the available iron, vitamin A, thiamin, riboflavin, and niacin served was consumed, the average intakes met the goal for most of the nutrients. School lunches and noon meals consumed at home were nutritionally superior to bag lunches from home. No significant differences were noted between school and home lunches.
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Ten patients with moderate to severe atopic dermatitis had increased levels of IgE in the blood and a reduced level of T cells with Fc receptors for IgG (T gamma). After pronase and trypsin digestion of Fc receptors, cultured T cells regenerated the Fc receptors, but preserved the difference between patients and controls. Neuraminidase treatment increased the T gamma-cell level in both patients and controls. Serum from patients with atopic dermatitis could not reduce the T gamma-cell expression in the controls. With regard to Fc receptors, no qualitative difference was observed between patients and controls, but a genuine quantitative difference accounts for the observed reduction of T gamma cells in blood.
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The natural killer cell activity was studied in 25 patients with primary, secondary, or latent syphilis before and after treatment. In primary syphilis natural killer cell activity was increased, especially in patients lacking circulating lipoidal antibodies. In patients who had become seroreactive in the lipoidal tests it was depressed in those with secondary and latent syphilis. The natural killer cell activity thus becomes activated by the syphilitic infection but is significantly reduced during progression of the disease. The importance of the natural killer cell activity in controlling syphilitic infection is questionable.