Abstract

Understanding the biology of inflammation occurring at the entheseal-bone insertion has led to a better knowledge of the main drivers of inflammation in spondyloarthropathies. The clinical efficacy of tumor necrosis factor-α (TNF-α) blockers strongly supports the idea that TNF-α is a key molecule. Yet 40% of patients do not respond appropriately, indicating that other pathways are likely involved in these illnesses. Targeting T cells through a blockade of costimulating (CD28) molecules does not help, and in experimental models of sacroiliitis, targeting interleukin 6 (IL-6) did not provide any useful evidence. Immunohistological and functional data suggest that B cells, Th17, or IL-17A might be important, and indeed preliminary data concerning drugs targeting B cells and IL-17A seem to suggest clinical benefits.

Links

Publisher Full Text

Authors

Ferraccioli G, Gremese E

Institution

Institute of Rheumatology, School of Medicine, Catholic University of the Sacred Heart, Rome, Italy. gf.ferraccioli@rm.unicatt.it

Source

The Journal of rheumatology. Supplement 89: 2012 Jul pg 94-6

MeSH

Animals
Anti-Inflammatory Agents
B-Lymphocytes
Bone and Bones
Drug Design
Humans
Interleukin-6
Joints
Molecular Targeted Therapy
Signal Transduction
Spondylarthropathies
Th17 Cells
Transforming Growth Factor beta1
Tumor Necrosis Factor-alpha

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

22751604