Gene/Protein
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Enzyme
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Gene/Protein
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Target Concepts:
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Query: UNIPROT:P14784 (
IL-2 receptor
)
3,849
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The evaluation of the changes of lymphocytes: T(CD3), B (CD19), subpopulations CD4, CD8, active lymphocytes CD3 + HLA-DR+, lymphocytes with the receptor for IL2(CD3 + CD25+), NK cells as well as the CD4/CD8 ratio in 30 patients with the early localized (group I n = 7) and early disseminated (group II n = 23) type of Lyme disease, before (examination 1) and after the antibiotic therapy (examination 2) was performed. Group III was composed of 90 healthy people. Measurements were carried out in an COULTER EPIC XL cytoflowmeter, using Becton Dickinson antibodies. Statistical analysis was performed using AnStat software. In the examined groups, a decrease of the subpopulations of CD4, CD8 lymphocytes in comparison with healthy subjects was revealed, as well as a decrease of the CD4/CD8 ratio after treatment. A considerably lower percentage value of active lymphocytes CD3 + HLA-DR+ in both groups and the reduction of the NK subpopulation before and after treatment of early disseminated Lyme disease in comparison with healthy people was observed. The higher percentage values of the lymphocytes with
IL-2 receptor
were not statistically significant. The indicated essential changes in the subpopulations of T lymphocytes, characterized by a decrease before the antibiotic therapy and by the tendency towards an increase after that therapy of the percentage of CD4, CD8, NK and CD3 + HLA-DR+ lymphocytes in peripheral blood, point out their role in the immunopathogenesis of the Lyme disease. The absence of the complete normalization of the examined parameters after the treatment, on the one hand, may provide evidence for some inertia of the elements of the immune system, on the other hand can also result from too short antibiotic therapy and maintenance of the antigenic stimulation.
Med Sci
Monit
PMID:Subpopulations of the peripheral lymphocytes in the early clinical forms of Lyme disease. 1120 23
SDZ RAD (everolimus, Certican is a novel macrolide immunosuppressant that blocks growth factor-driven transduction signals in the T-cell response to alloantigen. After stimulation of the
IL-2 receptor
on the activated T-cell, SDZ RAD inhibits p70S6 kinase, acting at a later stage in the T-cell mediated response than do cyclosporine and other calcineurin inhibitors (CNIs). Unlike the CNIs, SDZ RAD is a proliferation signal inhibitor, blocking growth factor-driven proliferation of both hematopoietic and nonhematopoietic cells. These activities are complementary to those of cyclosporine and provide a rationale for the addition of SDZ RAD to cyclosporine-based immunosuppression, with the potential for minimizing CNI nephrotoxicity, reducing the incidence of acute rejection, and favoring long-term graft survival. Potential also exists for beneficial effects on other factors that may influence the development of chronic rejection. These factors include comorbid diseases such as hypertension, which may affect transplant vasculopathy, and opportunistic infection with cytomegalovirus (CMV) and other viruses, which may increase the risk of chronic rejection. The synergistic effect of SDZ RAD and cyclosporine has been confirmed in preclinical models, with graft survival being significantly prolonged in rat models of kidney and heart allotransplantation. Clinical experience with SDZ RAD in cyclosporine-based immunosuppression, including low-dose cyclosporine regimens, has also resulted in predictable and favorable clinical outcomes. Low rates of acute rejection, excellent rates of patient and graft survival, lower incidence of CMV infections, better cholesterol, triglyceride and creatinine profiles, and better renal function have been demonstrated with SDZ RAD and lower doses of cyclosporine (Neoral; Novartis) in recipients of renal transplants. These findings, combined with good tolerability rates and an acceptable side-effect profile, indicate that the synergistic profile of SDZ RAD in combination with nontoxic dosages of CNI's and IL2 inhibitors will further improve longterm results in renal transplantation.
Ther Drug
Monit
2002 Feb
PMID:Early clinical experience with a novel rapamycin derivative. 1180 23
Interleukin 2 (IL-2), or T-cell growth factor (TCGF), represents the first identified, fully-characterized, purified human interleukin. It is produced mainly by T helper (CD4+) lymphocytes, stimulates cell-mediated immune responses, controls growth and differentiation of B lymphocytes, and intensifies proliferation and activity of all cytotoxic cell clones. IL-2 is a growth factor in vitro and a mediator of self-tolerance in vivo, and therefore interests tumor immunotherapy investigators. The role of IL-2 in the cell cycle of neoplastic cells remains unclear. IL-2 inhibits growth of certain human tumor cells while proliferation of other cells remains intact or is even stimulated. Decreased IL-2 production is often observed in the more advanced clinical stages of human tumors, which provides rational for inclusion of recombinant IL-2 in the immunotherapy for some tumors. On the other hand, tumor cells themselves may produce IL-2 and promote tumor growth. This article summarizes the current physiological role of IL-2 and its role in the pathogenesis of select human diseases. Many papers (including reviews) pertain to the IL-2R receptor. The soluble form of the alpha subunit of the
IL-2 receptor
(sIL-2Ralpha) is elevated in most proliferative disturbances of the hematopoietic system and in many solid tumors. Special reference to the most important discoveries and our own experience in intracellular detection of IL-2 and IL-2Ralpha are included. IL-2 properties, cellular sources, and targets, including data on its expression in pathological conditions, continue to be supplemented. Attempts to treat tumors are also discussed, using modified varieties of therapy that use IL-2 itself and/or its receptor.
Med Sci
Monit
2008 Oct
PMID:Biological properties of interleukin 2 and its role in pathogenesis of selected diseases--a review. 1883 Feb 8