Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of thymic humoral factor, THF, on systemic lupus erythematosus, SLE, lymphocyte function was investigated. Increasing numbers of SLE T-cells, rosetted at 4 degrees C or 37 degrees C, were cultured with allogeneic normal B-cells and the change in IgM synthesis was assessed. Lymphocytes of some SLE patients showed improved suppression with THF when rosetted at 37 degrees C. Normal control lymphocytes did not show a net change in suppression with THF. The subgroup of SLE patients that showed improved suppression with THF in vitro might be a more appropriate group for in vivo therapeutic trials with thymic hormone, TH, than SLE patients in general.
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PMID:The influence of thymic humoral factor on systemic lupus erythematosus lymphocyte function. 387

In systemic lupus erythematosus (SLE) is a disease characterized by B cell hyperactivity, autoantibody production and immune complex deposition in vital organs. To explain the mechanisms responsible for immune dysregulation in SLE cytokines have received increasing attention. This review has discussed a number of cytokines which appear to be involved in lupus pathogenesis. Recent studies have shown that disease activity and the main symptoms of SLE are associated with increasing serum levels of cytokines such as interleukin-(IL)-1, IL-2, IL-6, interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (THF-alpha). Constitutive expression and in vitro induction of specific cytokines are also aberrant in SLE. The presence of IL-1, IL-6 and IFN-gamma in involved kidneys suggests that they have local pathogenic effects. Moreover IFN-gamma, IL-6 and IL-1 modulate spontaneous IgG production by SLE mononuclear cells. During the next several years, the exact role of these cytokine in the pathogenesis of lupus become more fully elucidated.
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PMID:[Cytokines in systemic lupus erythematosus]. 899 65

In view of the documented association of solute carrier family 19 member 1 (SLC19A1) G80A (R27H) polymorphism with the risk for different types of cancers and systemic lupus erythematosus (SLE), we have reanalysed the case-control study on breast cancer to ascertain the conditions in which this polymorphic variant exerts the risk of breast cancer. Association statistics have revealed that this polymorphism exerts the risk for breast cancer under the conditions of low folate intake, and in the absence of well-documented protective polymorphism in cytosolic serine hydroxymethyltransferase. To substantiate this observation, we have developed a homology model of SLC19A1 using glycerol-3-phosphate transporter (d1pw4a) as a template where 73% of the residues were modelled at 90% confidence while 162 residues were modelled ab initio. The wild and mutant proteins shared same topology in S3, S5, S6, S7, S11 and S12 transmembrane domains. The topology varied at S1 (28-43 residue vs 28-44 residue), S2 (66-87 residue vs 69-87 residue), S4 (117-140 residue vs 117-139 residue), S8 (305-325 residue vs 305-324 residue), S9 (336-356 residue vs 336-355residue), and S10 (361-386 residue vs 361-385 residue) transmembrane domains between wild versus mutant proteins. S2 domain is shortened by three amino acid residues in the mutant while in other domains the difference corresponds to one amino acid residue. The 3DLigandSite analysis revealed that the metallic-ligand-binding sites at 273Trp, 277Asn, 379Leu, 439Phe and 442Leu are although unaffected, there is a loss of active sites corresponding to nonmetallic ligand binding. Tetrahydrofolate and methotrexate have lesser affinity towards the mutant protein than the wild protein. To conclude, the R27H polymorphism affects the secondary and tertiary structures of SLC19A1 with the significant loss in ligand-binding sites.
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PMID:In silico analysis of the structural and functional implications of SLC19A1 R27H polymorphism. 3154 89