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Resumen: BASICA Elisa Trujillo Martin
Hospital Universitario de Canarias, Tenerife.
Resumen: BASICA • Eje IL-17/23. IL-17/23, de la autoinmunidad a la inflamación. IL-17 y formación ósea en espondiloartritis.
• Microbiota/homeostasis intestinal y artritis. Microbioma y farmacomicrobiomica. Marcadores microbianos de actividad.
• Papel de HLA B27. Relación entre HLA B27 y microbiota intestinal.
• Nuevo mecanismo en la regeneración ósea. Netrin-1.
Novedades: vía IL-17/23. IL-17/23, de la autoinmunidad a la inflamación.
IL-17 y formación ósea en espondiloartritis.
IL-17/23 in transition from autoinmmunity to inflammation.
Pfeifle et al. Nat Immunol 2016, in press.
Pfeifle et al. Nat Immunol 2016, in press.
La IL-23 regula la actividad inflamatoria intrínseca de los anticuerpos. Regula la glicosilación de los anticuerpos. Regula la sialilacion de los anticuerpos.
IL-17/23 in transition from autoinmmunity to inflammation.
Pfeifle et al. Nat Immunol 2016, in press.
IL-17/23 in transition from autoinmmunity to inflammation.
Is there biological evidence supporting a role for IL-17 in new bone formation?
Is there biological evidence supporting a role for IL-17 in new bone formation?
Is there biological evidence supporting a role for IL-17 in new bone formation?
Is there biological evidence supporting a role for IL-17 in new bone formation?
Is there biological evidence supporting a role for IL-17 in new bone formation?
SUMMARY Structural damage in axial peripheral SpA is the result
of a combination of destruction and new bone formation.
Both TNF and IL-17 play a central role in osteoclast-mediated destruction, and bone destruction is halted by TNF1 as well as IL-17i in PsA.
The exact mechanisms of new bone formation remains partialy elusive, but increasing evidence indicates that IL-17 can induce bone formation in specific conditions.
Preliminary pre-clinical and clinical evidence suggests that IL-17 blockade may block bone formation in SpA.
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