Author: Mustafa, Maha; Vingsbo, Carina; Olsson, Tomas; Ljungdahl, Åke; Höjeberg, Bo; Holmdahl, Rikard
Title: The major histocompatibility complex influences myelin basic protein 63â€88â€induced T cell cytokine profile and experimental autoimmune encephalomyelitis Cord-id: yxw1r7ff Document date: 2005_12_11
ID: yxw1r7ff
Snippet: Polymorphism of the major histocompatibility complex (MHC) influences susceptibility to experimental autoimmune encephalomyelitis (EAE) induced by myelin basic protein (MBP) in rats. Current concepts relate such influences to the capacity of class II molecules to present relevant peptides to autoreactive T cells. We have here analyzed the MHC influence on the immune response and the development of EAE after immunization with the immunodominant peptide MBPâ€63–88. Analysis of MHCâ€congenic LE
Document: Polymorphism of the major histocompatibility complex (MHC) influences susceptibility to experimental autoimmune encephalomyelitis (EAE) induced by myelin basic protein (MBP) in rats. Current concepts relate such influences to the capacity of class II molecules to present relevant peptides to autoreactive T cells. We have here analyzed the MHC influence on the immune response and the development of EAE after immunization with the immunodominant peptide MBPâ€63–88. Analysis of MHCâ€congenic LEWIS strains showed that RT1(a), RT1(c) and RT1(l) haplotypes are permissive for disease induction, whereas RT1(d) and RT1(u) are resistant. All EAE responding strains showed peptideâ€specific proliferation and interferon (IFN)â€Î³ secretion, but no early significant tendency to express interleukin (ILâ€4) or transforming growth factor (TGF)â€Î² mRNA in lymphocytes in response to the MBP 63–88, 7 days post immunization (p.i.). Later, 14 days p.i., peptideâ€specific induction of ILâ€4 and TGFâ€Î² occurred in RT1(l) rats. Among the EAE nonâ€responders strains, only the RT1(u) rats showed an immune response to MBP 63â€88. This response, however, was qualitatively different from the immune response in the EAEâ€susceptible strains. Thus, there was no proliferation and only moderate IFNâ€Î³ production in response to peptide, but in contrast, a significant and early peptideâ€induced ILâ€4 and TGFâ€Î² response was observed. The data suggest that the MHCâ€associated susceptibility to EAE is partly related to the ability to mount a TH1â€like immune response while the MHCâ€associated EAE resistance may either be related to MBP peptide nonâ€responsiveness or to peptide recognition and induction of a qualitatively different and disease downâ€regulatory immune response.
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