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.