Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035412 (rhabdomyosarcoma)
 6,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The complement (C) system has previously been implicated in several diseases of muscle. We here report that human myoblasts or rhabdomyosarcoma cell lines spontaneously activate C through the classical pathway, causing release of anaphylatoxins and coating of myoblasts with opsonic C fragments but without causing cell killing. Survival of myoblasts is a consequence of the abundant expression of the membrane C regulatory molecules MCP and CD59, and neutralization of CD59 renders cells susceptible to C killing. The decay-accelerating factor was expressed at a very low level. Myoblasts and rhabdomyosarcoma lines also abundantly express the fluid-phase regulators C1-inhibitor, factor H, C4 binding protein, S-protein, and clusterin and secrete a soluble form of CD59. Expression of membrane and fluid-phase regulators is enhanced by either IFN-gamma or TNF-alpha. Although myoblasts resist C killing, spontaneous activation of C on these cells may have important consequences in inflammatory diseases of muscle where the generation of anaphylactic and opsonic fragments will recruit and activate inflammatory cells. C activation on myoblasts may also have consequences for the use of these cells as vehicles for gene delivery. Inhibition of C using soluble complement receptor I (sCR1) efficiently protected myoblasts from C attack in vitro, and this agent, already being tested in therapy of several C-mediated diseases, might be of value in inflammatory muscle disease and in improving the efficiency of gene delivery.
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PMID:Human skeletal myoblasts spontaneously activate allogeneic complement but are resistant to killing. 861 66

A number of echoviruses use decay accelerating factor (DAF) as a cellular receptor or attachment protein for cell infection. Binding of echovirus 7 to DAF at the cell surface, but not to soluble DAF in solution, triggers the formation of virus particles exhibiting an altered sedimentation coefficient ('A' particles) which are considered indicative of the particle uncoating process. We have previously demonstrated that antibodies to beta(2)-microglobulin block cell infection at a stage prior to 'A' particle formation and suggested that this reflects the involvement of beta(2)-microglobulin (or the associated MHC-I) in a virus-receptor complex that forms at the cell surface. We demonstrate here that antiserum to CD59 specifically blocks infection of rhabdomyosarcoma cells by a range of echoviruses, including viruses that bind DAF (e. g. echovirus 7) and those that use currently unidentified receptors other than DAF. The block occurs prior to 'A' particle formation and is cell-type specific. The potential role of CD59 as an active member, or passive participant, in the virus-receptor complex is discussed.
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PMID:Echovirus infection of rhabdomyosarcoma cells is inhibited by antiserum to the complement control protein CD59. 1076 83