Paraneoplastic myelopathy, neural autoantibody positive (Q100600): Difference between revisions

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Mielopatia paraneoplásica soropositiva para autoanticorpos neurais. Quando esses anticorpos neurais têm como alvo antígenos da membrana plasmática, eles são efetores de lesão (por exemplo, neuromielite óptica, que pode raramente se apresentar como um fenômeno paraneoplásico com soropositividade do anticorpo aquaporina-4) por meio de múltiplos mecanismos efetores. No entanto, quando alvejando antígenos nucleares ou citoplasmáticos (por exemplo, anfifisina-IgG ou proteína mediadora de resposta de colapsina-5-IgG [CRMP5-IgG ou anti-CV2), eles são marcadores de uma lesão mediada por efetor de células T, pois são inacessíveis ao ataque imunológico em situ, mas os peptídeos de proteínas intracelulares são exibidos em moléculas de MHC de classe 1 reguladas positivamente em um meio de citocinas pró-inflamatórias e, em seguida, acessíveis a células T citotóxicas específicas de peptídeo.
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Paraneoplastic myelopathy seropositive for neural autoantibodies. When these neural antibodies target plasma membrane antigens they are effectors of injury (e.g. neuromyelitis optica, which may rarely present as a paraneoplastic phenomenon with aquaporin-4 antibody seropositivity) through multiple effector mechanisms. However, when targeting nuclear or cytoplasmic antigens (e.g. amphiphysin-IgG or collapsin response mediator protein-5-IgG [CRMP5-IgG or anti-CV2) they are markers of a T-cell effector mediated injury as they are inaccessible to immune attack in situ, but peptides from intracellular proteins are displayed on upregulated MHC class 1 molecules in a pro-inflammatory cytokine milieu and then accessible to peptide specific cytotoxic T-cells.

Revision as of 17:19, 16 August 2026

Paraneoplastic myelopathy seropositive for neural autoantibodies. When these neural antibodies target plasma membrane antigens they are effectors of injury (e.g. neuromyelitis optica, which may rarely present as a paraneoplastic phenomenon with aquaporin-4 antibody seropositivity) through multiple effector mechanisms. However, when targeting nuclear or cytoplasmic antigens (e.g. amphiphysin-IgG or collapsin response mediator protein-5-IgG [CRMP5-IgG or anti-CV2) they are markers of a T-cell effector mediated injury as they are inaccessible to immune attack in situ, but peptides from intracellular proteins are displayed on upregulated MHC class 1 molecules in a pro-inflammatory cytokine milieu and then accessible to peptide specific cytotoxic T-cells.
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    Paraneoplastic myelopathy, neural autoantibody positive
    Paraneoplastic myelopathy seropositive for neural autoantibodies. When these neural antibodies target plasma membrane antigens they are effectors of injury (e.g. neuromyelitis optica, which may rarely present as a paraneoplastic phenomenon with aquaporin-4 antibody seropositivity) through multiple effector mechanisms. However, when targeting nuclear or cytoplasmic antigens (e.g. amphiphysin-IgG or collapsin response mediator protein-5-IgG [CRMP5-IgG or anti-CV2) they are markers of a T-cell effector mediated injury as they are inaccessible to immune attack in situ, but peptides from intracellular proteins are displayed on upregulated MHC class 1 molecules in a pro-inflammatory cytokine milieu and then accessible to peptide specific cytotoxic T-cells.

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