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Macrophage activation syndrome is a severe, potentially life-threatening, complication of several chronic rheumatic diseases of childhood. It occurs most commonly with systemic-onset juvenile idiopathic arthritis (SoJIA).
Macrophage activation syndrome. [3] Usual onset: 1-5 years old. [2] Diagnostic method: Excluding other disorders and clinical criteria. [2] Differential diagnosis: Septic arthritis, osteomyelitis, postinfectious arthritis, multisystem inflammatory syndrome in children, malignancy, and other autoimmune and autoinflammatory diseases. [2] Treatment
In rheumatic diseases, this syndrome is more often referred to as macrophage activation syndrome (MAS) and occurs most frequently in the juvenile onset and adult onset forms of Still's disease and in systemic lupus erythematosus. It occurs rarely in juvenile idiopathic arthritis, juvenile Kawasaki disease, and rheumatoid arthritis. [7]
The activation of T H 1 and M1 macrophage is a positive feedback loop, with IFN-γ from T H 1 cells upregulating CD40 expression on macrophages; the interaction between CD40 on the macrophages and CD40L on T cells activate macrophages to secrete IL-12; and IL-12 promotes more IFN-γ secretion from T H 1 cells.
Cytokine storm syndrome is a diverse set of conditions that can result in a cytokine storm. Cytokine storm syndromes include familial hemophagocytic lymphohistiocytosis , Epstein-Barr virus–associated hemophagocytic lymphohistiocytosis, systemic or non-systemic juvenile idiopathic arthritis –associated macrophage activation syndrome , NLRC4 ...
Macrophage activation syndrome, a potentially life-threatening complication of several chronic rheumatic diseases of childhood; The G protein-coupled receptor Mas, a critical part of the renin–angiotensin–aldosterone system (RAAS), encoded by the proto-oncogene MAS1; Mandibular advancement splint, a device used to treat sleep apnea
A macrophage-activating factor (MAF) is a lymphokine or other receptor based signal that primes macrophages towards cytotoxicity to tumors, cytokine secretion, or clearance of pathogens. Similar molecules may cause development of an inhibitory, regulatory phenotype.
The main marker of mast cell activation is inducible macrophage protein 1a (MIP-1α), which binds to mast cells when they are near each other. [9] After allergen exposure, MIP-1α transcription and expression are induced by resident mononuclear cells in the substantia propria, which consist of CD68+ macrophages and monocytes.