Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

OX40 belongs to the tumor necrosis factor receptor superfamily, and its expression is restricted to activated T-cells. Ligation of OX40 during T-cell-dendritic cell interaction is crucial for clonal expansion of antigen-specific T-cells and generation of T-cell memory. The ligand of OX40 (OX40L) is expressed not only on dendritic cells but also on other cell types, such as B-cells, vascular endothelial cells, natural killer cells, and mast cells. The pathophysiological relevance of this broad distribution needs further investigation. In particular, OX40L on vascular endothelial cells may play a role in inflammatory vasculitis as well as in atherosclerotic change. Recent studies with animal models have indicated the critical involvement of OX40 in the pathogenesis of a variety of immunologic abnormalities of inflammatory, autoimmune, infectious, allergic, and allotransplantation-related diseases. Blockade of OX40-OX40L interaction has been shown to prevent, cure, or ameliorate these diseases. In contrast, activation of OX40 is known to break an existing state of tolerance in malignancies, leading to a reactivation of antitumor immunity. These findings clearly suggest that the OX40/OX40L system is one of the most promising targets of immune intervention for treatment of these diseases.
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PMID:Roles of OX40 in the pathogenesis and the control of diseases. 1644 47

Henoch-Schonlein purpura (HSP) is one of the most common types of vasculitis disorders in childhood and is characterized by a rash, arthritis, abdominal pain, and renal involvement. T-lymphocyte activation is considered to play a critical role in vasculitis. However, the regulation of the T cells in HSP remains poorly understood. In this study, OX40/OX40L (CD134/CD252) costimulatory pathway, which could promote T-cell activation and long survival, was investigated. Results from 32 HSP patients and 25 healthy donors revealed that the freshly isolated CD4(+) T cells from patients with HSP expressed higher OX40 than that of the cells from healthy individuals. The levels of soluble OX40L (sOX40L) in the sera of patients with HSP were also much higher than the controls. Importantly, significantly elevated levels of OX40 on CD4(+) T cells and sOX40L in sera were detected in patients with HSP with nephritis compared to patients without nephritis, indicating both OX40 upregulation and sOX40L increase were closely associated with disease activity of the patients. Thus, circulating sOX40L could provide excessive costimulatory signal for CD4(+) OX40(+) T-cell activation, and OX40/OX40L signal might contribute to the development of HSP disease.
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PMID:Increased OX40 and soluble OX40 ligands in children with Henoch-Schonlein purpura: association with renal involvement. 2114 48