Paraneoplastic cerebellar degeneration, neural autoantibody positive (Q100596): Difference between revisions

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CID11:ID_351394127
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dki-india-ID_351394127
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Concluído
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Property / Knowledge Architect: https://pauloleads.com.br/cases-publicos/ / rank
 
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15 August 2026
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Latest 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);
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    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);

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      CID11:ID_351394127
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      dki-india-ID_351394127
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      Concluído
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      15 August 2026
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