FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2028332032> ?p ?o ?g. }

• W2028332032 endingPage "1638" @default.
• W2028332032 startingPage "1622" @default.
• W2028332032 abstract "Classical paraneoplastic encephalitis syndromes with 'onconeural' antibodies directed to intracellular antigens, and the recently described paraneoplastic or non-paraneoplastic encephalitides and antibodies against both neural surface antigens (voltage-gated potassium channel-complexes, N-methyl-d-aspartate receptors) and intracellular antigens (glutamic acid decarboxylase-65), constitute an increasingly recognized group of immune-mediated brain diseases. Evidence for specific immune mechanisms, however, is scarce. Here, we report qualitative and quantitative immunopathology in brain tissue (biopsy or autopsy material) of 17 cases with encephalitis and antibodies to either intracellular (Hu, Ma2, glutamic acid decarboxylase) or surface antigenic targets (voltage-gated potassium channel-complex or N-methyl-d-aspartate receptors). We hypothesized that the encephalitides with antibodies against intracellular antigens (intracellular antigen-onconeural and intracellular antigen-glutamic acid decarboxylase groups) would show neurodegeneration mediated by T cell cytotoxicity and the encephalitides with antibodies against surface antigens would be antibody-mediated and would show less T cell involvement. We found a higher CD8/CD3 ratio and more frequent appositions of granzyme-B(+) cytotoxic T cells to neurons, with associated neuronal loss, in the intracellular antigen-onconeural group (anti-Hu and anti-Ma2 cases) compared to the patients with surface antigens (anti-N-methyl-d-aspartate receptors and anti-voltage-gated potassium channel complex cases). One of the glutamic acid decarboxylase antibody encephalitis cases (intracellular antigen-glutamic acid decarboxylase group) showed multiple appositions of GrB-positive T cells to neurons. Generally, however, the glutamic acid decarboxylase antibody cases showed less intense inflammation and also had relatively low CD8/CD3 ratios compared with the intracellular antigen-onconeural cases. Conversely, we found complement C9neo deposition on neurons associated with acute neuronal cell death in the surface antigen group only, specifically in the voltage-gated potassium channel-complex antibody patients. N-methyl-d-aspartate receptors-antibody cases showed no evidence of antibody and complement-mediated tissue injury and were distinguished from all other encephalitides by the absence of clear neuronal pathology and a low density of inflammatory cells. Although tissue samples varied in location and in the stage of disease, our findings strongly support a central role for T cell-mediated neuronal cytotoxicity in encephalitides with antibodies against intracellular antigens. In voltage-gated potassium channel-complex encephalitis, a subset of the surface antigen antibody encephalitides, an antibody- and complement-mediated immune response appears to be responsible for neuronal loss and cerebral atrophy; the apparent absence of these mechanisms in N-methyl-d-aspartate receptors antibody encephalitis is intriguing and requires further study." @default.
• W2028332032 created "2016-06-24" @default.
• W2028332032 creator A5003170013 @default.
• W2028332032 creator A5003615920 @default.
• W2028332032 creator A5014342106 @default.
• W2028332032 creator A5019226669 @default.
• W2028332032 creator A5024681233 @default.
• W2028332032 creator A5042083351 @default.
• W2028332032 creator A5046643880 @default.
• W2028332032 creator A5050861407 @default.
• W2028332032 creator A5056148870 @default.
• W2028332032 creator A5060299317 @default.
• W2028332032 creator A5062939642 @default.
• W2028332032 creator A5074695558 @default.
• W2028332032 creator A5083946982 @default.
• W2028332032 date "2012-04-25" @default.
• W2028332032 modified "2023-10-11" @default.
• W2028332032 title "Immunopathology of autoantibody-associated encephalitides: clues for pathogenesis" @default.
• W2028332032 cites W1533919108 @default.
• W2028332032 cites W1967684158 @default.
• W2028332032 cites W1972725992 @default.
• W2028332032 cites W1974897738 @default.
• W2028332032 cites W1976986452 @default.
• W2028332032 cites W1978375913 @default.
• W2028332032 cites W1979087012 @default.
• W2028332032 cites W1981175379 @default.
• W2028332032 cites W1981234766 @default.
• W2028332032 cites W1983883744 @default.
• W2028332032 cites W1985489478 @default.
• W2028332032 cites W1986320586 @default.
• W2028332032 cites W2009224548 @default.
• W2028332032 cites W2014191362 @default.
• W2028332032 cites W2028092193 @default.
• W2028332032 cites W2046890475 @default.
• W2028332032 cites W2046908293 @default.
• W2028332032 cites W2048977435 @default.
• W2028332032 cites W2051552021 @default.
• W2028332032 cites W2055069215 @default.
• W2028332032 cites W2061056490 @default.
• W2028332032 cites W2072597173 @default.
• W2028332032 cites W2076409173 @default.
• W2028332032 cites W2076537666 @default.
• W2028332032 cites W2085856553 @default.
• W2028332032 cites W2089032704 @default.
• W2028332032 cites W2089967493 @default.
• W2028332032 cites W2100252544 @default.
• W2028332032 cites W2118067546 @default.
• W2028332032 cites W2121155292 @default.
• W2028332032 cites W2123159874 @default.
• W2028332032 cites W2124472369 @default.
• W2028332032 cites W2126193485 @default.
• W2028332032 cites W2127043216 @default.
• W2028332032 cites W2127990813 @default.
• W2028332032 cites W2130384971 @default.
• W2028332032 cites W2131625303 @default.
• W2028332032 cites W2133203361 @default.
• W2028332032 cites W2140152000 @default.
• W2028332032 cites W2141120827 @default.
• W2028332032 cites W2146199022 @default.
• W2028332032 cites W2147259071 @default.
• W2028332032 cites W2157802470 @default.
• W2028332032 cites W2159289827 @default.
• W2028332032 cites W2323257769 @default.
• W2028332032 cites W23834218 @default.
• W2028332032 cites W2410772780 @default.
• W2028332032 cites W4247974197 @default.
• W2028332032 cites W4252793583 @default.
• W2028332032 doi "https://doi.org/10.1093/brain/aws082" @default.
• W2028332032 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22539258" @default.
• W2028332032 hasPublicationYear "2012" @default.
• W2028332032 type Work @default.
• W2028332032 sameAs 2028332032 @default.
• W2028332032 citedByCount "501" @default.
• W2028332032 countsByYear W20283320322012 @default.
• W2028332032 countsByYear W20283320322013 @default.
• W2028332032 countsByYear W20283320322014 @default.
• W2028332032 countsByYear W20283320322015 @default.
• W2028332032 countsByYear W20283320322016 @default.
• W2028332032 countsByYear W20283320322017 @default.
• W2028332032 countsByYear W20283320322018 @default.
• W2028332032 countsByYear W20283320322019 @default.
• W2028332032 countsByYear W20283320322020 @default.
• W2028332032 countsByYear W20283320322021 @default.
• W2028332032 countsByYear W20283320322022 @default.
• W2028332032 countsByYear W20283320322023 @default.
• W2028332032 crossrefType "journal-article" @default.
• W2028332032 hasAuthorship W2028332032A5003170013 @default.
• W2028332032 hasAuthorship W2028332032A5003615920 @default.
• W2028332032 hasAuthorship W2028332032A5014342106 @default.
• W2028332032 hasAuthorship W2028332032A5019226669 @default.
• W2028332032 hasAuthorship W2028332032A5024681233 @default.
• W2028332032 hasAuthorship W2028332032A5042083351 @default.
• W2028332032 hasAuthorship W2028332032A5046643880 @default.
• W2028332032 hasAuthorship W2028332032A5050861407 @default.
• W2028332032 hasAuthorship W2028332032A5056148870 @default.
• W2028332032 hasAuthorship W2028332032A5060299317 @default.
• W2028332032 hasAuthorship W2028332032A5062939642 @default.
• W2028332032 hasAuthorship W2028332032A5074695558 @default.

• next