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Biomedical subjects

N Talal

Publications and source records attributed to N Talal.

At least 199 records · Page 11Linked to original sources
PubMed1981

[Stimulation of T-lymphocytes by autologous monocytes. Decrease in the proliferative response in Gougerot-Sjögren syndrome].

A mixed autologous culture enables the measurement of the proliferative response of T lymphocytes which have been stimulated by preparations of autologous mononucleated cells. The role of the monocytes present in the preparation was examined in this study which sought to determine if the autologous response induced by these monocytes was modified during Sjögren's syndrome. Purified monocytes are a powerful stimulant of autologous response in normal subjects. However, high concentrations of monocytes were found to have an inhibiting effect. In patients with Sjögren syndrome, the autologous response induced by monocytes in significantly decreased. This decrease parallels a reduction on "non-T" lymphocytes observed in these same patients. The anomaly provoking these two modifications does not appear to be caused by a seric factor or by a deficit of the proliferation of responding T lymphocytes. It is more likely due to a blockage of lymphocyte T/monocyte interactions where the markers of the HLA-D system intervene.

Cell Division↗
PubMed1981

Antibodies to polyadenylic acid in patients with myasthenia gravis.

Sera from 100 patients with myasthenia gravis and 45 patients with non-myasthenia gravis neuromuscular diseases were studied for antibodies to poly rA, poly rA-rU, native and denatured DNA. All patients with myasthenia gravis had significant anti-acetylcholine receptor antibodies with a mean titre of 1.2 X 10(-7)M. Forty-eight per cent of the myasthenia gravis patients had anti-poly rA antibody levels which were greater than 3 standard deviations from the mean of 65 control patients by Millipore filter radioimmunoassay. The antibody was specific for poly rA and present in a much higher frequency than antibodies to the other nucleic acids tested. Sucrose-gradient ultracentrifugation demonstrated that the antibody was limited to the IgM class alone. Mechanisms relating these findings to a more generalized immunological dysfunction are discussed.

Antibodies↗
PubMed1981

Natural killing by spleen cells from W/Wv and Sl/Sld anemic mice.

Natural killer cells are mononuclear cells that spontaneously lyse certain tumor cell lines without prior sensitization to the target. In mice, precursors of natural killer cells exist in the bone marrow. Moreover, natural killing is thought to be "marrow-dependent" because irradiation of the marrow in vivo with 89strontium reduces natural killing outside the marrow. We examined natural killing in W/Wv mice, which are congenitally anemic because of a defect in erythropoietic stem cells, and in congenitally anemic Sl/Sld mice, which have a defect in the host environment that prevents effective erythropoiesis. Young (6-8 week) W/Wv mice had reduced levels of natural killing when compared to their normal littermates. The defect in W/Wv mice is discussed in relation to their defects in erythropoiesis. Sl/Sld mice had normal levels of natural killing, demonstrating that the defect in erythropoietic environment does not affect the generation of NK cells.

Anemia↗
PubMed1981

Antibody-dependent cellular cytotoxicity in recurrent aphthous ulceration.

Antibody-dependent cellular cytotoxicity (ADCC) was investigated as s possible mechanism of pathogenesis in recurrent aphthous ulceration (RAU). ADCC induced by mononuclear cells from patients at various stages of RAU was compared with ADCC induced by mononuclear cells from paired controls. Chicken red blood cells (ChRBC) coated with rabbit anti-ChRBC antibody were used as targets. A significant increase in ADCC (P less than 0.01, paired sample t-test) in patients' samples as compared with controls was found only at the early stage of the disease. No increased cytotoxicity over control values was observed at any other single stage of the disease. The transient increased cytotoxicity observed in the early stage of RAU may reflect a number of possible mechanisms, including an increased number of ADCC effector cells only at the early stage, an increase in Fc receptor avidity, or an increase in efficiency of the existing effector cell population.

Adolescent↗
PubMed1980

Immune complexes in Sjögren's syndrome.

Sera from 48 patients with Sjögren's syndrome were examined for immune complexes by the Raji cell assay. There was no correlation between levels of immune complexes and the degree of lymphocytic infiltration of the labial salivary glands. Serum complement levels were normal. Five patients were serially followed during the development of pseudolymphoma or malignant lymphoma. Immune complex levels in 4 of the 5 patients were generally unchanged throughout the illness and did not parallel disease activity, rheumatoid factor, or SS-A and SS-B concentrations. Possible roles for immune complexes in Sjögren's syndrome are discussed.

Antibody Formation↗
PubMed1980

Decreased autologous mixed lymphocyte reaction in Sjögren's syndrome.

The autologous mixed lymphocyte reaction (AMLR) measures the response of peripheral blood T cells to antigens present on the surface of non-T cells. The AMLR was studied in 25 patients with Sjögren's syndrome (SS). The AMLR was decreased in 15 of 25 (60%) of patients with SS (5,272 +/- 6,738 cpm vs. 14,396 +/- 10,092 cpm for the normal controls, P < 0.001). The AMLR was decreased in 8 of 15 patients with only glandular disease who were not on any systemic medications. Patients with SS and associated disease had lower responses than patients with SS alone. Two patients with pseudolymphoma had absent response. The decreased AMLR correlated with a decreased response to concanavalin A, suggesting a possible abnormality of a T cell subpopulation. There was no correlation between the decreased AMLR and age, focus score, serum immunoglobulin concentration, the titer of antilymphocyte antibody, or phytohemagglutinin response. In allogeneic MLR, SS non-T cells and macrophages stimulated normal allogeneic T cells less well than normal non-T cells and macrophages, suggesting a possible abnormality in the cells that stimulate in the cells that stimulate in the allogeneic MLR.

Adult↗
PubMed1980

Circulating immune complexes in Takayasu disease.

Circulating immune complexes in Takayasu disease were investigated to assess the involvement of autoimmune mechanisms. Antibody dependent cell-mediated cytotoxicity (ADCC) and Raji cell assay revealed: The 10 percent inhibition of ADCC in 37 patients was 35.6 +/- 5.2, this being a non-statistically significant value as compared with the values of 25.6 +/- 3.0 in 33 apparently healthy controls. Raji cell assay values were 30.4 +/- 11.5 and 3.5 +/- 2.3 for patients and controls, respectively. As 54% of all these patients had a negative reaction and there was no correlation between immune complex levels and BSR, CRP, or ASO, immune complexes, while accelerating or modifying the pathophysiological state, probably are not primary causative factors.

Adult↗
PubMed1980

Antigen-specific factors produced by carrier-primed New Zealand Black mice.

We studied antigen-specific suppression in NZB and B/W mice to investigate immunoregulatory circuits associated with autoimmune disease. Young NZB and B/W mice produced ample suppressor factor, and acceptor cells were present even in older mice. A low m.w. antigen-specific enhancing factor capable of augmenting the secondary in vitro IgG antibody response to DNP was found. These results indicate the complexity of immunoregulation in these autoimmune-susceptible mice.

Aging↗
PubMed1980

Ability of NZW but not NZB antigen-presenting cells to support T cell proliferative response to DNA methylated albumin.

The genetic contribution of the parental NZB and NZW mouse to the antigen-induced, macrophage-dependent, lymph node T cell proliferative response to d-DNA-mBSA was studied in F1 hybrid NZB/NZW (B/W) mice. Mice were immunized subcutaneously in the tail with denatured DNA-methylated BSA. Primed T cells from these mice were obtained after passage of immune periaortic and inguinal lymph node cells through nylon wool. The primed T cells were exposed in vitro to d-DNA-mBSA presented on spleen cells from BALB/c, DBA/2, NZB, NZW, or B/W mice. Immune B/W T cells gave a substantial proliferative response only in the presence of antigen-presenting cells from B/W or NZW mice. These results suggest that the response of B/W mice to DNA occurs primarily through the NZW H-2 haplotype of their own antigen-presenting cells.

Animals↗