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• W1938595280 startingPage "1347" @default.
• W1938595280 abstract "Sporadic inclusion body myositis (IBM) is a muscle disease with two separate pathogenic components, degeneration and inflammation. Typically, nonnecrotic myofibers are focally surrounded and invaded by CD8⁺ T cells and macrophages. Both attacked and nonattacked myofibers express high levels of human leukocyte antigen class I (HLA-I) molecules, a prerequisite for antigen presentation to CD8⁺ T cells. However, only a subgroup of HLA-I⁺ myofibers is attacked by immune cells. By using IHC, we classified myofibers from five patients with sporadic IBM as attacked (A_IBM) or nonattacked (N_IBM) and isolated the intracellular contents of myofibers separately by laser microdissection. For comparison, we isolated myofibers from control persons (H_CTRL). The samples were analyzed by microarray hybridization and quantitative PCR. HLA-I up-regulation was observed in A_IBM and N_IBM, whereas H_CTRL were negative for HLA-I. In contrast, the inducible chain of the interferon (IFN) γ receptor (IFNGR2) and several IFN-γ–induced genes were up-regulated in A_IBM compared with N_IBM and H_CTRL fibers. Confocal microscopy confirmed segmental IFNGR2 up-regulation on the membranes of A_IBM, which positively correlated with the number of adjacent CD8⁺ T cells. Thus, the differential up-regulation of the IFN-γ signaling cascade observed in the attacked fibers is related to local inflammation, whereas the ubiquitous HLA-I expression on IBM muscle fibers does not require IFNGR expression." @default.
• W1938595280 created "2016-06-24" @default.
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• W1938595280 date "2011-09-01" @default.
• W1938595280 modified "2023-10-09" @default.
• W1938595280 title "Inclusion Body Myositis" @default.
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• W1938595280 doi "https://doi.org/10.1016/j.ajpath.2011.05.055" @default.
• W1938595280 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3157228" @default.
• W1938595280 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21855683" @default.
• W1938595280 hasPublicationYear "2011" @default.
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