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.
MeSH terms
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Animals
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Anti-Inflammatory Agents / therapeutic use*
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B-Lymphocytes / drug effects
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B-Lymphocytes / immunology
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Bone and Bones / drug effects
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Bone and Bones / immunology
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Bone and Bones / pathology
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Drug Design
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Humans
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Interleukin-6 / antagonists & inhibitors
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Interleukin-6 / metabolism
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Joints / drug effects*
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Joints / immunology
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Joints / pathology
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Molecular Targeted Therapy*
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Signal Transduction / drug effects
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Spondylarthropathies / drug therapy*
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Spondylarthropathies / immunology
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Spondylarthropathies / pathology
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Th17 Cells / drug effects
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Th17 Cells / immunology
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Transforming Growth Factor beta1 / antagonists & inhibitors
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Transforming Growth Factor beta1 / metabolism
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Tumor Necrosis Factor-alpha / antagonists & inhibitors*
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Anti-Inflammatory Agents
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Interleukin-6
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Transforming Growth Factor beta1
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Tumor Necrosis Factor-alpha