Insights into FcγR involvement in pain-like behavior induced by an RA-derived anti-modified protein autoantibody

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AudienciaPúblico en generales_ES
CoberturaMéxicoes_ES
Fecha de ingreso2026-10-05T16:33:34Z
Fecha de publicación2023-01-01
ResumenJoint pain is one of the most debilitating symptoms of rheumatoid arthritis (RA) and patients frequently rate improvements in pain management as their priority. RA is hallmarked by the presence of anti-modified protein autoantibodies (AMPA) against post-translationally modified citrullinated, carbamylated and acetylated pro-teins. It has been suggested that autoantibody-mediated processes represent distinct mechanisms contributing to pain in RA. In this study, we investigated the pronociceptive properties of monoclonal AMPA 1325:01B09 (B09 mAb) derived from the plasma cell of an RA patient. We found that B09 mAb induces pain-like behavior in mice that is not associated with any visual, histological or transcriptional signs of inflammation in the joints, and not alleviated by non-steroidal anti-inflammatory drugs (NSAIDs). Instead, we found that B09 mAb is retained in dorsal root ganglia (DRG) and alters the expression of several satellite glia cell (SGC), neuron and macrophage-related factors in DRGs. Using mice that lack activating Fc \& gamma;Rs, we uncovered that Fc \& gamma;Rs are critical for the development of B09-induced pain-like behavior, and partially drive the transcriptional changes in the DRGs. Finally, we observed that B09 mAb binds SGC in vitro and in combination with external stimuli like ATP enhances transcriptional changes and protein release of pronociceptive factors from SGCs. We propose that certain RA antibodies bind epitopes in the DRG, here on SGCs, form immune complexes and activate resident macrophages via Fc \& gamma;R cross-linking. Our work supports the growing notion that autoantibodies can alter nociceptor signaling via mechanisms that are at large independent of local inflammatory processes in the joint.es_ES
Doihttps://doi.org/10.1016/j.bbi.2023.07.001es_ES
URIhttps://riuat.uat.edu.mx/handle/123456789/5395
Idiomaenes_ES
EditorialACADEMIC PRESS INC ELSEVIER SCIENCEes_ES
RelaciónBrain, Behavior, and Immunityes_ES
URL relacionadohttps://doi.org/10.1016/j.bbi.2023.07.001es_ES
DerechosAcceso abierto (Metadatos de producción científica)es_ES
Licenciahttp://purl.org/coar/access_right/c_abf2es_ES
FuenteBrain, Behavior, and Immunity
Palabra clavePaines_ES
Palabra claveAutoantibodieses_ES
Palabra claveDorsal root gangliaes_ES
Palabra claveSatellite glia cellses_ES
Palabra claveRheumatoid arthritises_ES
TítuloInsights into FcγR involvement in pain-like behavior induced by an RA-derived anti-modified protein autoantibodyes_ES
TipoArtículoes_ES
ArbitradoHa sido Arbitradoes_ES
AutorJurczak, Alexandra
AutorSandor, Katalin
AutorFarinotti, Alex Bersellini
AutorKrock, Emerson
AutorHunt, Matthew A.
AutorAgalave, Nilesh M.
AutorBarbier, Julie
AutorSimon, Nils
AutorWang, Zhenggang
AutorRudjito, Resti
AutorVazquez-Mora, Juan Antonio
AutorMartinez-Martinez, Arisai
AutorRaoof, Ramin
AutorEijkelkamp, Niels
AutorGronwall, Caroline
AutorKlareskog, Lars
AutorJimenez-Andrade, Juan Miguel
AutorMarchand, Fabien
AutorSvensson, Camilla I.
AutorJurczak, Alexandraes_ES
AutorSandor, Katalines_ES
AutorFarinotti, Alex Bersellinies_ES
AutorKrock, Emersones_ES
AutorHunt, Matthew A.es_ES
AutorAgalave, Nilesh M.es_ES
AutorBarbier, Juliees_ES
AutorSimon, Nilses_ES
AutorWang, Zhengganges_ES
AutorRudjito, Resties_ES
AutorVazquez-Mora, Juan Antonioes_ES
AutorMartinez-Martinez, Arisaies_ES
AutorRaoof, Ramines_ES
AutorEijkelkamp, Nielses_ES
AutorGronwall, Carolinees_ES
AutorKlareskog, Larses_ES
AutorJimenez-Andrade, Juan Migueles_ES
AutorMarchand, Fabienes_ES
AutorSvensson, Camilla I.es_ES
InstituciónUniversidad Autónoma de Tamaulipas
InstituciónUniversidad Autónoma de Tamaulipases_ES
Rango de páginas212-227es_ES
URL relacionadahttps://doi.org/10.1016/j.bbi.2023.07.001
Tipo de artículoIndexado
Tipo de artículoIndexadoes_ES
Volumen113es_ES

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