Paraneoplastic movement disorder, autoantibody positive (Q100620): Difference between revisions
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Transtorno de movimento paraneoplásico soropositivo para autoanticorpos neurais. Quando esses anticorpos neurais têm como alvo antígenos da membrana plasmática, eles são causas de lesão (por exemplo, receptor de N-metil-D-aspartato associado a teratomas ovarianos) por meio de múltiplos mecanismos efetores. No entanto, ao alvejar antígenos nucleares ou citoplasmáticos (por exemplo, colapsina-resposta-mediador-proteína-5 [CRMP5] coréia paraneoplásica associada a câncer de pulmão de células pequenas e timoma), eles são marcadores de uma lesão mediada por efetores de células T, pois são inacessíveis ao ataque imune in 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 peptídeos._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); GABABR (autoanticorpos de ácido gama-aminobutírico); NMDA-R (autoanticorpos para o receptor de N-metil-D-aspartato); Ma2; | |||
| description / en | description / en | ||
Paraneoplastic movement disorder seropositive for neural autoantibodies. When these neural antibodies target plasma membrane antigens they are causes of injury (e.g. N-methyl-D-aspartate receptor associated with ovarian teratomas) through multiple effector mechanisms. However, when targeting nuclear or cytoplasmic antigens (e.g. collapsin-response-mediator-protein-5 [CRMP5] paraneoplastic chorea associated with and small-cell lung cancer and thymoma) 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); GABABR (Gamma-aminobutyric-acid autoantibodies); NMDA-R (N-methyl-D-aspartate receptor autoantibodies); Ma2; | |||
Revision as of 17:21, 16 August 2026
Paraneoplastic movement disorder seropositive for neural autoantibodies. When these neural antibodies target plasma membrane antigens they are causes of injury (e.g. N-methyl-D-aspartate receptor associated with ovarian teratomas) through multiple effector mechanisms. However, when targeting nuclear or cytoplasmic antigens (e.g. collapsin-response-mediator-protein-5 [CRMP5] paraneoplastic chorea associated with and small-cell lung cancer and thymoma) 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); GABABR (Gamma-aminobutyric-acid autoantibodies); NMDA-R (N-methyl-D-aspartate receptor autoantibodies); Ma2;
| Language | Label | Description | Also known as |
|---|---|---|---|
| default for all languages | ID_502185974 |
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| English | Paraneoplastic movement disorder, autoantibody positive |
Paraneoplastic movement disorder seropositive for neural autoantibodies. When these neural antibodies target plasma membrane antigens they are causes of injury (e.g. N-methyl-D-aspartate receptor associated with ovarian teratomas) through multiple effector mechanisms. However, when targeting nuclear or cytoplasmic antigens (e.g. collapsin-response-mediator-protein-5 [CRMP5] paraneoplastic chorea associated with and small-cell lung cancer and thymoma) 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); GABABR (Gamma-aminobutyric-acid autoantibodies); NMDA-R (N-methyl-D-aspartate receptor autoantibodies); Ma2; |
