Paraneoplastic brainstem encephalitis, neural autoantibody positive (Q100579): Difference between revisions
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Encefalite paraneoplásica de tronco cerebral 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, quando almejando antígenos nucleares ou citoplasmáticos (por exemplo, anticorpo nuclear antineuronal tipo 2 [ANNA-2 ou anti-Ri] associado a cânceres de pulmão e de mama), eles são marcadores de uma lesão mediada por células T efetoras, 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_ AMPA-R (anticorpos do receptor do ácido amino-3-hidroxi-5-metil-4-isoxazolpropiônico); anfifisina; ANNA-1 (anti-Hu) (auto-anticorpo nuclear antineuronal tipo 1); ANNA-2 (anti-Ri) (autoanticorpo nuclear antineuronal tipo 2); ANNA-3 (auto-anticorpo nuclear antineuronal tipo 3); CRMP5 (anti-CV2) (proteína 5 do mediador da resposta da colapsina); GABABR (autoanticorpos de ácido gama-aminobutírico tipo A); Ma1; Ma2; | |||
| description / en | description / en | ||
Paraneoplastic brainstem encephalitis 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. antineuronal nuclear antibody type 2 [ANNA-2 or anti-Ri] associated with lung and breast cancers) 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: AMPA-R (amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antibodies); amphiphysin; ANNA-1(anti-Hu) (antineuronal nuclear autoantibody type 1); ANNA-2(anti-Ri) (antineuronal nuclear autoantibody type 2); ANNA-3 (antineuronal nuclear autoantibody type 3); CRMP5(anti-CV2) (collapsin response mediator protein 5); GABABR (Gamma-aminobutyric-acid type-A autoantibodies); Ma1; Ma2; | |||
Revision as of 17:18, 16 August 2026
Paraneoplastic brainstem encephalitis 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. antineuronal nuclear antibody type 2 [ANNA-2 or anti-Ri] associated with lung and breast cancers) 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: AMPA-R (amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antibodies); amphiphysin; ANNA-1(anti-Hu) (antineuronal nuclear autoantibody type 1); ANNA-2(anti-Ri) (antineuronal nuclear autoantibody type 2); ANNA-3 (antineuronal nuclear autoantibody type 3); CRMP5(anti-CV2) (collapsin response mediator protein 5); GABABR (Gamma-aminobutyric-acid type-A autoantibodies); Ma1; Ma2;
| Language | Label | Description | Also known as |
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| default for all languages | ID_1483064286 |
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| English | Paraneoplastic brainstem encephalitis, neural autoantibody positive |
Paraneoplastic brainstem encephalitis 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. antineuronal nuclear antibody type 2 [ANNA-2 or anti-Ri] associated with lung and breast cancers) 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: AMPA-R (amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antibodies); amphiphysin; ANNA-1(anti-Hu) (antineuronal nuclear autoantibody type 1); ANNA-2(anti-Ri) (antineuronal nuclear autoantibody type 2); ANNA-3 (antineuronal nuclear autoantibody type 3); CRMP5(anti-CV2) (collapsin response mediator protein 5); GABABR (Gamma-aminobutyric-acid type-A autoantibodies); Ma1; Ma2; |
