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S Ragheb

Publications and source records attributed to S Ragheb.

12 recordsLinked to original sources
PubMed1994

Interleukin-1 alpha, but not interleukin-1 beta, is a co-mitogen for neonatal rat Schwann cells in vitro and acts via interleukin-1 receptors.

The culture of neonatal rat Schwann cells (SC) with unfractionated cytokines induces an increase in SC proliferation. Previous studies demonstrated that while incubation of SC with interleukin-1(IL-1) does not result in enhanced SC mitogenesis, a mixture of antibodies to IL-1 alpha plus IL-1 beta inhibits cytokine-induced proliferation. We undertook the current studies to: (i) confirm that neither isoform of IL-1 directly causes SC proliferation; (ii) determine if there is a difference in the effect of antibodies to IL-1 alpha versus IL-1 beta; and (iii) determine if IL-1 contribution to cytokine-induced proliferation of SC is mediated via IL-1 receptors. IL-1 alpha or IL-1 beta from several sources, over a wide range of concentrations, failed to induce SC proliferation. Polyclonal antibodies to IL-1 alpha from several suppliers and a monoclonal antibody to IL-1 alpha inhibited SC proliferation, whereas similar antibodies to IL-1 beta had no effect on cytokine-induced SC proliferation. Addition of excess IL-1 alpha to an incubation mixture of unfractionated cytokines plus anti-IL-1 alpha abolished the inhibitory effect of the antibodies. Addition of IL-1 receptor antagonist (IL-1 Ra) to unfractionated cytokines inhibited SC proliferation. Therefore, while neither IL-1 alpha nor IL-1 beta is a solitary mitogen for neonatal rat SC, IL-1 alpha but not IL-1 beta acts as a co-mitogen. Moreover, IL-1 alpha seems to exert its co-mitogenic effect via receptors for IL-1.

Animals↗
PubMed1992

Effect of clinical status and treatment on the frequency of CD5+ B cells in patients with myasthenia gravis.

CD5+ B cells comprise a subset of B lymphocytes that may play a pathogenetic role in the development of human autoimmune disease. We previously reported a high-frequency phenotype (greater than 30% CD5+ B cells) in the peripheral blood of 57% of myasthenia gravis (MG) patients and 13% of controls. We have now examined additional patients (n = 41) and controls (n = 27) and continue to find that 44% of MG patients have a high-frequency phenotype of CD5+ B cells compared with 7% of controls. Serial studies showed that the frequency of CD5+ B cells in peripheral blood remained fairly stable for controls and that it may decrease with immunosuppressive therapy of MG patients. In patients receiving anticholinesterase only or no therapy (n = 21), the age at onset of MG, presence or absence of detectable serum anti-acetylcholine receptor antibody, clinical extent of MG, and the duration of disease may affect the frequency of CD5+ B cells in the blood.

Adult↗
PubMed1990

Recombinant IL-2 therapy reverses diminished granulomatous responsiveness in anti-L3T4-treated, Schistosoma mansoni-infected mice.

We have previously shown, that anti-L3T4 mAb treatment strongly suppressed granuloma formation in the liver, and IL-2 production in the spleen of Schistosoma mansoni-infected mice. In the present study the dynamics of IL-2 production was delineated during the infection, and the effect of rIL-2 treatment on granulomatous responsiveness was examined. IL-2 production in soluble egg Ag-stimulated spleen cells of mice was detectable at 6, peaked at 8 and waned by 20 wk of the infection. In contrast, Con A stimulus elicited high levels of IL-2 production by 8 wk which remained nearly unchanged throughout the infection. Administration of rIL-2 to acutely infected, anti-L3T4 mAb-treated, or chronically infected mice reversed the diminished or modulated granulomatous responses without restoring the ability for endogenous IL-2 production. Transfer of spleen cells of anti-L3T4 mAb-treated, chronically infected mice did not indicate a role for Ts cells in the impaired production of IL-2 in recipients. These data suggest that lack of IL-2 production can play an important role in the immunoregulation of the granulomatous response.

Animals↗
PubMed1990

Interactions between adherent mononuclear cells and lymphocytes from granulomas of mice with schistosomiasis mansoni.

T-lymphocyte-adherent mononuclear cell interaction was analyzed in the vigorous and immunomodulated liver granulomas of Schistosoma mansoni-infected mice. Collagenase-dispersed granulomas contained 15% lymphocytes, 30% macrophages, 50% eosinophilis, and some neutrophils. Dispersed granuloma cells stimulated with concanavalin A or soluble worm egg antigens (SEA) did not proliferate unless plate-adherent, esterase-positive mononuclear cells were removed before culture. To analyze the granuloma adherent cell-mediated suppression, vigorous granuloma cell cultures partially depleted of adherent mononuclear cells were supplemented with indomethacin, catalase, superoxide dismutase, levamisole, and anti-murine alpha/beta interferon antiserum. In concanavalin A and SEA-stimulated cultures, only the addition of indomethacin or anti-alpha/beta interferon antiserum alleviated the adherent cell-mediated suppression of vigorous granuloma lymphocyte response. In contrast, these agents only minimally alleviated the suppressed response of SEA-stimulated, immunomodulated granuloma lymphocytes. Moreover, coculture of equal numbers of vigorous and immunomodulated granuloma cells partially depleted of adherent suppressor cells abrogated the alleviated response of vigorous granuloma lymphocytes. These findings indicate that, within the schistosome egg-induced vigorous granulomas, the adherent mononuclear cells exert regulation over lymphocyte responsiveness by alpha/beta-interferon and an indomethacin-sensitive, probably prostaglandin-mediated pathway. Within the immunomodulated granulomas, the adherent suppressor cell-mediated regulation of lymphocyte proliferation appears to play a lesser role.

Animals↗
PubMed1990

The frequency of CD5+ B lymphocytes in the peripheral blood of patients with myasthenia gravis.

A subset of human B lymphocytes expresses Leu-1 (CD5), a pan-T cell marker, which is the equivalent of the murine Lyt-1 molecule. CD5+ B cells produce autoantibodies in vitro; therefore, they may play a role in the pathogenesis of autoimmune disorders. In myasthenia gravis (MG), autoantibodies are directed against the nicotinic acetylcholine receptor (AChR) at the neuromuscular junction. We examined the peripheral blood leukocytes of MG patients (n = 21) and controls (n = 15) for the presence of Leu-1+ B lymphocytes. A fraction of B-1 (CD20)+ cells expressed Leu-1 at a low density. There was a statistically significant difference in the frequency of Leu-1+ B cells between patients and controls. We observed 2 frequency ranges of Leu-1+ B cells (0 to 30% and above 30%), which were not related to the total percentage of B-1+ cells in the blood. Fifty-seven percent of MG patients had a high frequency of Leu-1+ B cells compared with 13% of controls.

Adult↗
PubMed1989

Characterization of granuloma T lymphocyte function from Schistosoma mansoni-infected mice.

This study was undertaken to characterize and compare T lymphocyte function from the vigorous and modulated liver granulomas of Schistosoma mansoni-infected mice. Although both types of lesion contained equal percentages of T lymphocytes, the T cell subset distribution was different. For vigorous lesions, the ratio of helper/effector to suppressor/cytotoxic T cells was 2 to 3:1. For modulated lesions the ratio was lower (1:1). Differences in the phenotypic profiles of vigorous and modulated granuloma (Gr) T cells were reflected in their functional activity. Vigorous Gr T cells were more active in lymphoproliferation, IL-2 production, and granuloma formation than those from modulated lesions. Moreover, modulated Gr T cells suppressed the functional activity of vigorous Gr T cells in a dose-dependent manner. The selective depletion of T cell subsets showed that phenotypically, the Gr delayed-hypersensitivity T cell is L3T4+, Lyt-1+ whereas the Gr Ts cell is an Lyt-2+ lymphocyte. Both of these T cell subsets are present in vigorous and modulated lesions. During acute infection, delayed-hypersensitivity T cell lymphocyte functions predominate, whereas Ts lymphocyte functions appear to prevail during chronic infection.

Animals↗
PubMed1987

Establishment and characterization of an antigen-specific T-cell line from liver granulomas of Schistosoma mansoni-infected mice.

Granulomatous inflammations in schistosomiasis mansoni are the result of T-cell-mediated reactions to soluble egg antigens (SEA) secreted by parasite ova. To study TDH effector cell function, a granuloma T-cell line was established from collagenase-digested liver granulomas of acutely infected CBA/J mice. Dispersed nonadherent granuloma cells were cultured with feeder layer cells and SEA or with feeder layer cells alone in alternate cycles for 32 weeks. The granuloma T-cell line was L3T4+ Lyt-1+. In vitro, the SEA-stimulated T cells showed proliferation and interleukin 2 production. One million T cells adoptively transferred SEA-specific footpad swelling, and 7.5 X 10(6) T cells adoptively transferred granulomatous hypersensitivity to injected ova or SEA-coated beads. Anti-L3T4 monoclonal antibody blocked the SEA-specific cell proliferation. Depletion of L3T4+ cells abrogated, while that of Lyt-1+ cells diminished the adoptive transfer of SEA-specific footpad swelling. These experiments demonstrate that the granuloma T-lymphocyte population contains TDH-type effector cells. Establishment of an SEA-specific granuloma T-cell line will allow the study of the effector functions of the hitherto uncharacterized intralesional granuloma T lymphocyte.

Animals↗