Paraneoplastic cerebellar degeneration, neural autoantibody positive (Q100596): Difference between revisions
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Degeneração cerebelar paraneoplásica soropositiva para autoanticorpos neurais. Quando esses anticorpos neurais têm como alvo antígenos da membrana plasmática, eles são efetores de lesão (por exemplo, autoanticorpos complexos de canais de potássio controlados por voltagem) por meio de múltiplos mecanismos efetores. No entanto, ao alvejar antígenos nucleares ou citoplasmáticos (por exemplo, autoanticorpo de célula de Purkinje tipo 1 [PCA-1 ou anti-Yo] mais frequentemente associado a tumores ovarianos), eles são marcadores de uma lesão mediada por efetores 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._x000D_ _x000D_ Os autoanticorpos neurais associados incluem:_x000D_ _x000D_ ANNA-2 (anti-Ri) (autoanticorpo nuclear antineuronal tipo 2); CRMP5 (anti-CV2) (proteína 5 do mediador da resposta da colapsina); mGluR1 (anticorpo metabotrópico para o receptor de glutamato tipo 1); GABABR (autoanticorpos do tipo B de ácido gama-aminobutírico); Ma1; Ma2; PCA-1 (anti-Yo) (autoanticorpo citoplasmático de células de purkinje tipo 1); PCA-2 (autoanticorpo citoplasmático de células de purkinje tipo 2); PCA-Tr (autoanticorpo de células purkinje-Tr); | |||
| description / en | description / en | ||
Paraneoplastic cerebellar degeneration seropositive for neural autoantibodies. When these neural antibodies target plasma membrane antigens they are effectors of injury (e.g. voltage gated potassium channel complex autoantibodies) through multiple effector mechanisms. However, when targeting nuclear or cytoplasmic antigens (e.g. Purkinje cell autoantibody type 1 [PCA-1 or anti-Yo] most frequently associated with ovarian tumours) 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. Associated neural autoantibodies include: ANNA-2(anti-Ri) (antineuronal nuclear autoantibody type 2); CRMP5(anti-CV2) (collapsin response mediator protein 5); mGluR1 (metabotropic glutamate receptor antibody type 1); GABABR (Gamma-aminobutyric-acid type-B autoantibodies); Ma1; Ma2; PCA-1(anti-Yo) (purkinje cell cytoplasmic autoantibody type 1); PCA-2 (purkinje cell cytoplasmic autoantibody type 2); PCA-Tr (purkinje cell autoantibody-Tr); | |||
Revision as of 17:19, 16 August 2026
Paraneoplastic cerebellar degeneration seropositive for neural autoantibodies. When these neural antibodies target plasma membrane antigens they are effectors of injury (e.g. voltage gated potassium channel complex autoantibodies) through multiple effector mechanisms. However, when targeting nuclear or cytoplasmic antigens (e.g. Purkinje cell autoantibody type 1 [PCA-1 or anti-Yo] most frequently associated with ovarian tumours) 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. Associated neural autoantibodies include: ANNA-2(anti-Ri) (antineuronal nuclear autoantibody type 2); CRMP5(anti-CV2) (collapsin response mediator protein 5); mGluR1 (metabotropic glutamate receptor antibody type 1); GABABR (Gamma-aminobutyric-acid type-B autoantibodies); Ma1; Ma2; PCA-1(anti-Yo) (purkinje cell cytoplasmic autoantibody type 1); PCA-2 (purkinje cell cytoplasmic autoantibody type 2); PCA-Tr (purkinje cell autoantibody-Tr);
| Language | Label | Description | Also known as |
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| default for all languages | ID_351394127 |
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| English | Paraneoplastic cerebellar degeneration, neural autoantibody positive |
Paraneoplastic cerebellar degeneration seropositive for neural autoantibodies. When these neural antibodies target plasma membrane antigens they are effectors of injury (e.g. voltage gated potassium channel complex autoantibodies) through multiple effector mechanisms. However, when targeting nuclear or cytoplasmic antigens (e.g. Purkinje cell autoantibody type 1 [PCA-1 or anti-Yo] most frequently associated with ovarian tumours) 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. Associated neural autoantibodies include: ANNA-2(anti-Ri) (antineuronal nuclear autoantibody type 2); CRMP5(anti-CV2) (collapsin response mediator protein 5); mGluR1 (metabotropic glutamate receptor antibody type 1); GABABR (Gamma-aminobutyric-acid type-B autoantibodies); Ma1; Ma2; PCA-1(anti-Yo) (purkinje cell cytoplasmic autoantibody type 1); PCA-2 (purkinje cell cytoplasmic autoantibody type 2); PCA-Tr (purkinje cell autoantibody-Tr); |
