Publications by authors named "Kermani-Arab V"

The defective clearance of amyloid-beta (Abeta) in the brain of Alzheimer's disease (AD) patients is unexplained. The immunohistochemical studies of the frontal lobe and hippocampus show perivascular and intraplaque infiltration by blood-borne macrophages containing intracellular Abeta but only inefficient clearance of beta deposits. Neurons and neuronal nuclei, respectively, express interleukin-1beta and the chemokine RANTES, which could induce the inflammatory cell infiltration.

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Objectives: Productive Herpesviridae infections are implicated in the etio-pathogenesis of aggressive periodontitis. However, virtually nothing is known about a possible role of herpesviruses in pulpal and periapical pathosis. This study employed a cDNA analysis to determine transcription of human cytomegalovirus (HCMV), Epstein-Barr virus (EBV) and herpes simplex virus (HSV) in 14 recalcitrant periapical lesions and in 2 periapical healthy control sites.

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Histamine inhibited the proliferative response of human peripheral blood mononuclear cells (PBMC) to the T cell mitogen Phytohemagglutinin-P (PHA-P) in a dose-dependent fashion. This inhibition was mediated via the H2 receptor since cimetidine, a known H2 antagonist, removed the inhibition, whereas the addition of the H1 antagonist Diphenhydramine did not. Inhibition occurred during the inductive phase of the cell cycle, since histamine added 24 hours after PHA-P stimulation had no effect on subsequent T cell proliferation, and was attributable to inhibition of interleukin-2 (IL-2) gene expression.

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We have developed a simple protocol for the routine purification of essentially homogeneous human interleukin 2. The procedures applied include ammonium sulfate precipitation, ACA-54 gel filtration, ultrafiltration and chromatofocusing. The product has a molecular weight of 14 000, as determined by electrophoretic mobility, and is free of interleukin 1, interferon, granulocyte and monocyte stimulating factors, B cell growth factor and phytohemagglutinin.

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The active form of vitamin D3, 1 alpha,25-dihydroxyvitamin D3 (1,25-(OH)2-D3), suppresses in vitro immunoglobulin (Ig) production by activated peripheral blood mononuclear cells (PBM) from normal human subjects by inhibiting T helper/inducer TH cell activity. Normal PBM were fractionated into B, TH and T suppressor/cytotoxic (Ts) cells by fluorescence-activated cell sorting techniques. The resultant subsets were activated with mitogens and were cultured in the presence or absence of a receptor-saturating concentration of 1,25-(OH)2-D3.

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Normal human peripheral blood mononuclear cells (PBMC) were cultured with phytohemagglutinin-P (PHAP) and cyclosporine (CsA) to investigate the mode of action of CsA on cellular proliferation. CsA at 1 microgram/ml exerted a marked inhibitory effect on PBMC responsiveness to PHAP. An antiproliferative effect of CsA was observed at the inductive phase of the cell cycle, but the drug was ineffective when it was added to cultures 24 hr after stimulation.

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Because interleukin 2 (IL 2) production and IL 2 receptor (IL 2R) expression are essential steps in T cell proliferation, we undertook to measure these parameters, as defects in one or both seemed likely to account for the reduced proliferative response to mitogen in acquired immune deficiency syndrome (AIDS) and lymphadenopathy syndrome (LAS). Reduced proliferative responses to PHA are a well established feature of AIDS with opportunistic infection (AIDS-OI), AIDS with Kaposi's sarcoma (AIDS-KS), and LAS patient groups. IL 2R expression was significantly reduced in both AIDS groups; a similar trend was observed with the LAS group.

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Peripheral blood mononuclear cells from 22 pemphigus patients with active disease and 30 normal subjects were evaluated for interleukin 2 (IL-2) production and IL-2 receptor expression following stimulation with phytohemagglutinin P (PHA-P). The IL-2 levels were lower in patients compared to corresponding controls and the production was delayed after PHA stimulation. This deficiency was most pronounced in severely affected patients.

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Peripheral blood lymphocytes obtained at various intervals from normal individuals and from a patient with mycosis fungoides (MF) were cultured with phytohemagglutinin (PHA) for 3 days to activate suppressor cells. After being cultured, the PHA-treated cells were irradiated, washed, and then transferred to fresh medium with PHA. The PHA responsiveness of the cells from normal individuals was suppressed approximately 90% by autologous or normal allogeneic lymphocytes activated for 3 days with PHA, whereas the cells activated for 3 days with PHA from the patient with MF lacked the capacity to inhibit the mitogenic response of autologous or allogeneic lymphocytes.

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The relative frequency of peripheral blood T and B cells and their biological function(s) from a group of patients with pityriasis rosea (PR) was investigated during the acute and convalescent phases of the disease using rosetting, immunofluorescent tests, and in vitro cell culturing with anti-delta and anti-mu antibodies and phytohemagglutinin (PHA). The total number of immunoglobulin (Ig) bearing cells was significantly increased, in conjunction with a slight decrease in the T cell population. Lymphocytes with surface IgD, IgM, or both Ig, accounted for the increase in the B cell population.

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Specifically purifed anti-human delta stimulated the in vitro incorporation of [3H]thymidine by human peripheral lymphocytes from patients with chronic lymphocytic leukaemia (CLL). The peak response varied between individuals; those with 5--52% IgD-bearing lymphocytes exhibited maximum stimulation at 3 days, whereas a patient with only 1% IgD-bearing cells showed optimal activation at 6 days. In agreement with others, our data indicated that, in most instances, lymphocytes from patients with CLL respond poorly to PHA.

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Human peripheral lymphocytes were stimulated to incorporate tritiated thymidine when cultured with anti-sigma. The stimulation of lymphocytes by anti-sigma inversely correlates to PHA-induced lymphocyte transformation. In addition, lymphocytes from individuals with low serum IgD levels exhibited a significant response to anti-sigma, whereas, those with normal or slightly elevated levels of serum IgD showed minimal stimulation.

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Human peripheral lymphocytes with the capacity to be stimulated by anti-delta exhibited in PHA responsiveness when cultured with anti-delta 1 or 12 hr before PHA exposure over cells exposed to PHA alone. When these lymphocytes were preincubated with PHA 1 or 12 hr before anti-delta activation, no augmentation of the PHA response was seen. In addition, lymphocytes from donors with a high PHA response (low anti-delta activation) failed to show an enhancing effect on PHA responsiveness when pretreated with anti-delta.

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Bursa- and thymus-dependent functions were examined in Marek's disease (MD)-susceptible normal chickens and in chickens treated with 5 and 16 mg of cyclophosphamide (CY) at the time of hatching. Chickens not exposed to Marek's disease virus (MDV) and treated with CY temporarily lost mitogenic response to concanavalin A but regained full response after 5 weeks. Bursa-dependent functions, such as presence of germinal centers in spleen and cecal tonsils, morphologic features of bursa, and sheep red blood cell antibody response were completely lost in chickens treated with 16 mg of CY and only partly retained in chickens treated with 5 mg of CY.

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The effects of passive immunization with immunoglobulin Y (IgY) on the pathogenesis of Marek's disease (MD) were examined in an experimental line of White Leghorn chickens highly susceptible to MD. Purified IgY with anti-MDV antibody activity, when injected into chicks, delayed the development of MDV viremia and lesions until 9 days postinoculation (PI) with Marek's disease virus (MDV). The blastogenic response of spleen cells to concanavallin-A was depressed at 6 days PI in the birds without passive immunization, whereas it was not totally depressed until 17 days in birds passively immunized with IgY anti-MDV antibody.

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The levels of IgM, IgY, and IgA and the development of specific antibody to Marek's disease virus (MDV) and sheep red blood cells (SRBC) in young chickens susceptible and resistant to Marek's disease were compared after exposure to MDV. No significant difference was noted in the immunoglobulin levels. However, the antibody response to MDV and SRBC occurred more rapidly in susceptible birds.

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The effect of cyclophosphamide on the pathogenesis of Marek's disease was examined in a line of chickens which is relatively resistant to Marek's disease. The injection of cyclophosphamide into newly hatched chickens delayed and reduced viremia and also reduced the development of Marek's disease lesions until 2 weeks after exposure to Marek's disease virus. The data indicate that a population of T cells susceptible to infection with virus and possibly viral transformation is affected by cyclophosphamide.

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The effect of passive immunization with immunoglobulin Y (IgY) antibody against Marek's disease virus (MDV) was examined in MDV-susceptible chickens. The production of IgY, immunoglobulin M, and probably also immunoglobulin A was depressed in passively immunized chickens when compared with that in MDV-exposed chickens which had not been given IgY anti-MDV antibody. In passively immunized chickens, the synthesis of immunoglobulin M and IgY anti-MDV antibodies in response to MDV infection also was delayed as determined by agar gel precipitin and indirect fluorescence antibody tests.

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