Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P14784 (IL-2 receptor)
 3,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixty eight patients with verified multiple sclerosis (MS) (mean EDSS score 3.1 +/- 1.0) and 50 healthy donors have been investigated. Thirty five patients had relapsing-remitting, 25--secondary progressive, 8--primary progressive course. The remission was in 38, decompensation--in 20, relapse--in 10 patients. Lymphocyte subpopulations were investigated using monoclonal antibodies (Moscow) to the following antigens: CD3 (T-lymphocytes), CD4 (T-helpers), CD8 (T-supressors), CD20 (8-lymphocytes), CD25 (IL-2 receptor), CD16 (natural killers), CD95 (activated cells ready to apoptosis). Cytokines and tumor necrosis factor-alpha (TNF-alpha) levels were measured using ELISA test. HLA antigens were investigated by standard lymphocytotoxic test. In MS we found a fall of CD3, CD4, CD8, CD20 and CD16, but an increase of CD4/CD8, CD95, CD25. The CD95 level correlated with CD4, CD4/CD8 and CD16. In MS spontaneous IL-2, IL-6, IL-8 and TNF-alpha production was raised and stimulated IL-6 and IL-8 secretion was reduced. IL-4, IL-6, IL-8, TNF-alpha and IL-1 beta serum production in vivo was elevated. We found an increase of CD3, CD4, CD16, CD25, but a decrease of IL-1 (p < 0.01) spontaneous production and IL-6, IL-8, TNF-a stimulated secretion in DR2(+) MS patients, comparing to DR2(-) patients and controls. In DR2(-) patients as compared to DR2(+) patients and controls, all lymphocyte subpopulations levels, especially CD8 (p < 0.001) one, were decreased, but spontaneous IL-8 (p < 0.01) production was increased. The data obtained indicate lymphocyte apoptosis activation, targeting promoted lymphocyte destruction, and suggest T helper type-1 reaction prevalence in MS.
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PMID:[Immunogenetic cytokine restriction in multiple sclerosis]. 1158 2

Fibromyalgia and chronic hepatitis C infection share many clinical features including prominent somatic complaints such as musculoskeletal pain and fatigue. There is a growing body of evidence supporting a link between cytokines and somatic complaints. This review discusses alterations of cytokines in fibromyalgia, including increased serum levels of interleukin (IL)-2, IL-2 receptor, IL-8, IL-1 receptor antagonist; increased IL-1 and IL-6 produced by stimulated peripheral blood mononuclear cell in patients with FM for longer than 2 years; increased gp130, which is a neutrophil cytokine transducing protein; increased soluble IL-6 receptor and soluble IL-1 receptor antagonist only in patients with fibromyalgia who are depressed; and IL-1 beta, IL-6, and TNF-a by reverse transcriptase-polymerase chain reaction in skin biopsies of some patients with fibromyalgia. In addition, this review describes the mechanism by which alterations in cytokines in fibromyalgia and chronic hepatitis C infection can produce hyperalgesia and other neurally mediated symptoms through the presence of cytokine receptors on glial cells and opiate receptors on lymphocytes and the influence of cytokines on the hypothalamus-pituitary-adrenal axis such as IL-1, IL-6, and TNF-a activating and IL-2 and IFN-a down-regulating the HPA axis, respectively. The association between chronic hepatitis C infection and fibromyalgia is discussed, including a description of key cytokine changes in chronic hepatitis C infection. Future studies are encouraged to further characterize these immunologic alterations with potential pathophysiologic and therapeutic implications.
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PMID:Fibromyalgia, hepatitis C infection, and the cytokine connection. 1294 86