Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:BIOD00082 (IL-2)
 29,198 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of treatment with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and vitamin E, an antioxidant, on immune functions were examined. Male C57/B1 mice were fed daily with natural vitamin E for 12 weeks, subsequently injected i.p. with MPTP or its vehicle, and sacrificed 1 week later. Control mice received the stripped corn oil vehicle daily, in place of vitamin E. Oral vitamin E feeding increased cerebral vitamin E content by 60% (P = 0.05). However, MPTP attenuated this rise in cerebral vitamin E content when measured 1 week after treatment with the neurotoxin (P = 0.05). MPTP also produced an 80-90% reduction in striatal dopamine content in both the stripped corn oil control group and the vitamin E-treated group (P = 0.0000). One week after MPTP injection, the numbers of peripheral blood lymphocytes and the percent of spleen T-cells, but not B-cells, were decreased in those groups receiving MPTP alone or MPTP plus vitamin E (P less than 0.05 and 0.02, respectively). The Con A-induced IL-2 production of spleen cells was decreased in all treated groups (P less than 0.005). There was no difference in the mitogenic stimulative response to PHA, Con A or LPS. However, the response to PWM was increased in both MPTP and MPTP plus vitamin E-treated groups (P less than 0.05 and 0.001, respectively). On the other hand, the one-way mixed lymphocyte response of the splenocytes from the MPTP-treated group was increased (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of MPTP and vitamin E treatments on immune function in mice. 151 70

The effect of vitamin E supplementation on the immune response of healthy older adults was studied in a double-blind, placebo-controlled trial. Subjects (n = 32) resided in a metabolic research unit and received placebo or vitamin E (800 mg dl-alpha-tocopheryl acetate) for 30 d. Alpha-tocopherol content of plasma and peripheral blood mononuclear cells (PBMCs), delayed-type hypersensitivity skin test (DTH), mitogen-stimulated lymphocyte proliferation, as well as interleukin (IL)-1, IL-2, prostaglandin (PG) E2, and serum lipid peroxides were evaluated before and after treatment. In the vitamin E-supplemented group 1) alpha-tocopherol content was significantly higher (p less than 0.0001) in plasma and PBMCs, 2) cumulative diameter and number of positive antigen responses in DTH response were elevated (p less than 0.05), 3) IL-2 production and mitogenic response to optimal doses of concanavalin A were increased (p less than 0.05), and 4) PGE2 synthesis by PBMCs (p less than 0.005) and plasma lipid peroxides (p less than 0.001) were reduced. Short-term vitamin E supplementation improves immune responsiveness in healthy elderly individuals; this effect appears to be mediated by a decrease in PGE2 and/or other lipid-peroxidation products.
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PMID:Vitamin E supplementation enhances cell-mediated immunity in healthy elderly subjects. 200 77

Murine retrovirus infection induces loss of vitamin E and immune dysfunction with loss of cytokine production by T-helper cells. Therefore interferon-gamma (IFN-gamma) was given during dietary vitamin E supplementation to effectively prevent murine retrovirus-induced immunosuppression, cytokine dysregulation, and development of murine AIDS. Administration of IFN-gamma during vitamin E supplementation significantly prevented development of retrovirus-induced suppression of splenic natural killer cell activity and T cell proliferation. It also significantly slowed retrovirus-induced elevation of T helper (Th) 2 cytokine [interleukin (IL)-4, IL-5, and IL-10] production and monokine (IL-6 and tumor necrosis factor-alpha) secretion by splenocytes. The treatment also prevented loss of Th1 cytokine (IL-2 and IFN-gamma) secretion by splenocytes from retrovirus-infected mice alleviating splenomegaly and hypergammaglobulinemia. The combined therapy had an additive therapeutic impact. It was more effective than IFN-gamma treatment or vitamin E supplementation alone in delaying the development of retrovirus-induced immunosuppression with its cytokine dysregulation.
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PMID:Vitamin E supplementation with interferon-gamma administration retards immune dysfunction during murine retrovirus infection. 749 68

Female C57BL/6 mice were infected with LP-BM5 retrovirus, causing murine AIDS, which is functionally similar to human AIDS. Vitamin E effects on immune functions, cytokine production and nutritional concentrations in retrovirus-infected mice were determined. Retrovirus infection inhibited release of interleukin-2 (IL) and interferon-gamma (IFN) and some immune functions, whereas it stimulated secretion of IL-4, IL-5, IL-6 and tumor necrosis factor-alpha (TNF) and immunoglobulin (Ig) production. Furthermore, retrovirus infection induced some nutritional deficiencies in the tissues. A 15-fold increase in dietary vitamin E largely restored concentrations of some micronutrients (vitamins A and E, zinc and copper) in the liver, intestine, serum and thymus. It also partially restored production of IL-2 and IFN-gamma by splenocytes. Retrovirus-induced elevated production of IL-4, IL-5 and IL-6 by splenocytes in vitro was normalized by vitamin E. Elevated release of IL-6, TNF-alpha, IgA and IgG produced by splenocytes in vitro during murine AIDS were also completely or partially normalized by vitamin E. Vitamin E also prevented retrovirus-induced suppression of splenocyte proliferation and natural killer cell activity. These data indicate that vitamin E supplementation during murine AIDS can help to ameliorate the disorders during murine AIDS, suggesting vitamin E usefulness in treatment of AIDS in humans.
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PMID:Nutritional status and immune responses in mice with murine AIDS are normalized by vitamin E supplementation. 793 12

Female C57BL/6 mice were infected with LP-BM5 retrovirus, causing murine AIDS which is functionally similar to human AIDS. Retrovirus infection targets the thymus producing altered T-cell differentiation via the dysregulation of thymocyte cytokine production. Therefore the effects of dietary vitamin E at various levels were determined on cytokine production by ConA-stimulated thymocytes from uninfected (normal) and retrovirus-infected mice. Dietary supplementation, with a 15-, 150- and 450-fold increase of vitamin E in the diet modulated interleukin-2 (IL) production in both uninfected mice and retrovirus-infected mice. The 150- and 450-fold vitamin E supplementation significantly reduced IL-4 secretion by thymocytes from the uninfected, normal mice. Supplementation at all levels also significantly reduced IL-4 production by thymocytes, which was elevated by the retrovirus infection. Vitamin E significantly reduced IL-6 and interferon-gamma production increased during the progression to murine AIDS. The effects of dietary vitamin E on conA-induced proliferation of thymocytes were consistent with the finding on changes of IL-2 secretion. No effect of dietary vitamin E on thymus weight was observed in both uninfected and retrovirus-infected mice. These data indicate that dietary vitamin E supplementation at extremely high levels can modulate cytokine production by thymocytes. This could affect T-cell differentiation, especially during murine AIDS when cytokine production was partially normalized by vitamin E supplementation.
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PMID:Vitamin E supplementation at various levels alters cytokine production by thymocytes during retrovirus infection causing murine AIDS. 794 Jun 43

Female C57BL/6 mice were infected with LP-BM5 retrovirus, causing murine AIDS, which is functionally similar to human AIDS. Retrovirus infection targeted the thymus, producing altered T cell differentiation via the dysregulation of thymocyte cytokine production. Human AIDS causes vitamin deficiencies, therefore the effects of dietary vitamin E supplementation were determined on the kinetics of cytokine production by concanavalin A-stimulated thymocytes in uninfected normal mice and mice with murine AIDS. Dietary supplementation, with a 15-fold increase in vitamin E (160 IU/l) in the liquid diet (National Research Council), modulated interleukin-2 (IL) production in both uninfected mice and retrovirus-infected mice. Vitamin E significantly reduced the level of IL-4 secretion in the uninfected mice at 4 and 8 weeks, but not at 12 and 16 weeks. It also significantly reduced IL-4 production, elevated by retrovirus infection. Vitamin E significantly reduced IL-6, and interferon-gamma production increased in murine AIDS. The effects of dietary vitamin E on concanavalin A-induced proliferation of thymocytes were consistent with the finding of changes in IL-2 secretion. No effects of dietary vitamin E on thymus weight were observed in uninfected or retrovirus-infected mice, whereas vitamin E significantly increased serum and thymic vitamin E concentration, which had been reduced by retrovirus infection. These data indicate that dietary vitamin E supplementation can modulate cytokine production by thymocytes, affecting T cell differentiation, especially during retrovirus-induced immune dysfunction.
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PMID:Vitamin E supplementation modulates cytokine production by thymocytes during murine AIDS. 815 Nov 59

Vitamin E, an essential lipid-soluble micronutrient, plays an important role in the immune system and serves as an immunostimulant in geriatric subjects. Using an in vitro incubation to simulate aging processes, we find that vitamin E mitigates loss of growth capacity in lymphocytes. Vitamin E presence during in vitro incubation did not affect significantly the level of peroxidation, the effects of exogenous IL-2, PGE2, or indomethacin, nor levels of IL-2 production. Thus, the preservative effect on lymphocyte growth by vitamin E is not due primarily to its antioxidant function or to interleukin-2 or prostaglandin effects. The decreased growth capacity generated by in vitro incubation is accompanied by a variety of cellular alterations, including decreased CD5 surface antigen, enhanced suppression by adherent cells, and impaired communication between lymphocytes and adherent cells. The decrease in CD5 surface antigen correlates inversely with the cell density required for maximal cell proliferation, and the diminished CD5 levels were unaltered by vitamin E presence during the aging process. In contrast, protection of T-cell proliferative capacity by vitamin E in vitro correlates with diminished suppression by adherent cells and normalized interaction between lymphocytes and adherent cells.
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PMID:Protective effect of vitamin E on lymphocyte growth capacity during incubation in vitro. 853 42

The effects of polyunsaturated fatty acids (PUFAs: docosahexaenoic (DHA) and eicosapentaenoic (EPA) acids) on induced lymphocyte proliferation and expression of CD25alpha chain of interleukin-2 receptor, CD71 and HLA-DR were investigated. PUFAs had no effect on phytohaemagglutinin (PHA)-induced lymphocyte agglutination, but they strongly inhibited the lymphoproliferative response to PHA. This inhibitory effect is PUFA dose-dependent and seems to be more potent with DHA than EPA, Pre-incubation experiments showed that lymphocytes cultured with PUFAs for 6 h then washed and exposed to PHA, still inhibited lymphocyte proliferation. The authors also showed that this inhibitory activity was time dependent but became nonsignificant when PUFAs were added after 48 h lymphocyte culture. The addition of excess exogenous human recombinant rIL-2 partly restored PHA-lymphocyte proliferation inhibited by EPA but not by DHA. On the other hand, the authors showed that PUFAS did not inhibit IL-2 stimulated lymphocyte proliferation. The addition of PUFAs to cell culture medium had no inhibitory action on the PHA-induced lymphocyte expression of CD25, CD71 and HLA-DR. Furthermore, this effect appeared independent of eicosanoid synthesis or peroxide formation. Indeed, the inclusion of aspirin and vitamin E in the culture medium did not prevent the inhibitory effects of PUFAs on lymphocyte proliferation. Regardless of the mechanism of action, the inhibitory effect of PUFAs on activated lymphocytes may explain why some clinical trials of fish oil supplemented diets containing high amounts of DHA and EPA have been successful in improving the health status of patients suffering from inflammatory and autoimmune disorders.
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PMID:Docosahexaenoic and eicosapentaenoic acids inhibit human lymphoproliferative responses in vitro but not the expression of T cell surface activation markers. 860 57

Nutrition and nutritional status can have profound effects on immune functions, resistance to infection and autoimmunity in man and other animals. Nutrients enhance or depress immune function depending on the nutrient and level of its intake. Protein-energy malnutrition and vitamin A deficiency are strongly associated with impaired immunity and infectious disease. The essential role vitamin A plays in infection and maintenance of mucosal surfaces has long been known. Recent evidence shows that T-cell subpopulations, cytokines and antibody subclasses are all affected by vitamin A. In animal studies supplementation with vitamin E protects against infection and is linked to stimulatory effects on the immune system. In man vitamin E and other anti-oxidants increase the number of CD4+ cells. Dietary lipids and zinc have a substantial impact on autoimmunity from protective to potentiation of immuno-pathological processes in animals. There is considerable potential to modify human autoimmune disease by manipulation of lipid nutrition. Deficiency of pyridoxine induces atrophy of lymphoid organs, marked reduction in lymphocyte numbers, impairs antibody responses and IL-2 production. Dietary copper is important in the prevention of infection in some animal species and T-cell function is defective under deficiency states due to an inability to produce IL-2. Selenium has been linked to viral infection, enhanced T-cell functions and TNF beta induced increase in natural killer cell activity. Understanding the molecular and cellular immunological mechanisms involved in nutrient-immune interactions will increase our applications for nutrition of the immune system in health and in disease
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PMID:Nutrition and immunity with emphasis on infection and autoimmune disease. 873 70

To test whether T cell receptor (TCR) peptide treatment can prevent immune dysfunction, excessive lipid peroxidation, and malnutrition caused by retrovirus infection, female C57BL/6 mice were infected with LP-BM5 retrovirus. Infection with retrovirus inhibited lymphocyte proliferation, cytokine release T helper 1 cells, stimulated cytokine secretion by T helper 2 cells, induced abnormal hepatic and cardiac lipid profiles, and produced excessive tissue lipid peroxidation with hepatic and cardiac vitamin E deficiency. Two weeks after infection, TCR peptides Vbeta5.2, Vbeta8.1, Vbeta8.1 + Vbeta5.2, Vbeta8.1(N), and Vbeta8.1 were injected to the mice at dose of 200 microg/mouse. Vbeta8.1 and Vbeta5.2 treatments largely maintained lymphocyte proliferation and IL-2 and IFN-gamma release, and prevented excessive IL-6, IL-10, and TNF-alpha secretion. Concomitantly, these treatments normalized hepatic and cardiac lipid profiles, reduced tissue lipid peroxidation, and thereby significantly maintained vitamin E in the liver and heart. Vbeta8.1 segments treatment did not prevent the immune dysfunction, abnormal lipid profile and lipid peroxidation, and vitamin E deficiency caused by the retrovirus infection. In conclusion, injection of intact TCR peptides during murine retrovirus infection largely prevented immune dysfunction by blocking the excessive stimulation of a T cell subset caused by retroviral superantigens. It also ameliorated malnutrition status by normalizing lipid profile, lipid peroxidation, and vitamin E deficiency. T cell immune dysfunction and its prevention by TCR peptide treatment is important in the therapy of vitamin E deficiency induced by retrovirus infection.
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PMID:Prevention of retrovirus-induced aberrant cytokine secretion, excessive lipid peroxidation, and tissue vitamin E deficiency by T cell receptor peptide treatments in C57BL/6 mice. 901 66


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