Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interleukin 17 (IL-17) is a proinflammatory cytokine that has been the focus of intensive research because of its crucial role in the pathogenesis of different diseases across many medical specialties. In this context, the present review in which a panel of 13 experts in immunology, dermatology, rheumatology, neurology, hematology, infectious diseases, hepatology, cardiology, ophthalmology and oncology have been involved, puts in common the mechanisms through which IL-17 is considered a molecular target for the development of novel biological therapies in these different fields. A comprehensive review of the literature and analysis of the most outstanding evidence have provided the basis for discussing the most relevant data related to IL-17A blocking agents for the treatment of different disorders, such as psoriasis, psoriatic arthritis, rheumatoid arthritis, ankylosing spondylitis, cardiovascular disorders, non alcoholic fatty liver disease, multiple sclerosis, inflammatory bowel disease, uveitis, hematological and solid cancer. Current controversies are presented giving an opening line for future research.
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PMID:Critical role of interleukin (IL)-17 in inflammatory and immune disorders: An updated review of the evidence focusing in controversies. 3173 2

Discitis/ Osteomyelitis is an inflammatory process involving an intervertebral disc and the adjacent vertebral bodies. Infection is the most common cause of discitis, which is often spontaneous and hematogenous in origin. However, many noninfectious processes affecting the spine such as pseudarthrosis in ankylosing spondylitis, amyloidosis, destructive spondyloarthropathy of hemodialysis, Modic changes type 1, neuropathic arthropathy, calcium pyrophosphate dehydrate (CPPD) spondyloarthropathy and gout can mimic infectious discitis/ osteomyelitis. To determine whether a particular patient's spinal process is due to an infectious versus non-infectious cause can be challenging. Although clinical findings and laboratory studies including erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) can be helpful in the diagnosis of bacterial discitis/osteomyelitis due to their high sensitivity; however, their specificity is low. Moreover, both the infectious and non-infectious discitis can appear quite similar on the imaging studies. We present two cases of thoracic discitis with adjacent vertebral osteomyelitis of probable non-infectious etiology. Both were managed with instrumented fusion for stabilization. We also discuss a range of noninfectious causes of discitis/spondylitis and their radiological features which can help differentiate from infectious processes.
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PMID:Non-infectious thoracic discitis: A diagnostic and management dilemma. A report of two cases with review of the literature. 3193 36

The killer immunoglobulin-like receptors (KIRs), found predominantly on the surface of natural killer (NK) cells and some T-cells, are a collection of highly polymorphic activating and inhibitory receptors with variable specificity for class I human leukocyte antigen (HLA) ligands. Fifteen KIR genes are inherited in haplotypes of diverse gene content across the human population, and the repertoire of independently inherited KIR and HLA alleles is known to alter risk for immune-mediated and infectious disease by shifting the threshold of lymphocyte activation. We have conducted the largest disease-association study of KIR-HLA epistasis to date, enabled by the imputation of KIR gene and HLA allele dosages from genotype data for 12,214 healthy controls and 8,107 individuals with the HLA-B*27-associated immune-mediated arthritis, ankylosing spondylitis (AS). We identified epistatic interactions between KIR genes and their ligands (at both HLA subtype and allele resolution) that increase risk of disease, replicating analyses in a semi-independent cohort of 3,497 cases and 14,844 controls. We further confirmed that the strong AS-association with a pathogenic variant in the endoplasmic reticulum aminopeptidase gene ERAP1, known to alter the HLA-B*27 presented peptidome, is not modified by carriage of the canonical HLA-B receptor KIR3DL1/S1. Overall, our data suggests that AS risk is modified by the complement of KIRs and HLA ligands inherited, beyond the influence of HLA-B*27 alone, which collectively alter the proinflammatory capacity of KIR-expressing lymphocytes to contribute to disease immunopathogenesis.
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PMID:Epistatic interactions between killer immunoglobulin-like receptors and human leukocyte antigen ligands are associated with ankylosing spondylitis. 3280 49


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