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In type I diabetes, IL-13 antagonized cytotoxic insults to pancreatic β cells enhanced by IL-6. [22] In a mouse model of acetaminophen-induced liver injury eosinophil-driven IL-4/IL-13 mediated hepatoprotective function. [23] In severe alcohol-associated hepatitis low plasma level of IL-13 is a predictor of short-term (90-day) mortality. [24]
Activated STAT6 molecules form dimers which translocate to the nucleus to bind responsive elements (e.g. CD23 promoter in B cells, [12] arginase1 enhancer in macrophages [13]) The binding affinity of IL-4 for IL-4Rα is much higher than IL-13 for the IL-13Rα1, hence IL-4 would out-compete IL-13 for receptor availability within IL4R2 at parity ...
Interleukin 10 (IL-10) is a protein that inhibits the synthesis of a number of cytokines, including IFN-gamma, IL-2, IL-3, TNF, and GM-CSF produced by activated macrophages and by helper T cells. In structure, IL-10 is a protein of about 160 amino acids that contains four conserved cysteines involved in disulphide bonds. [33]
Interleukin 13 receptor, alpha 1, also known as IL13RA1 and CD213A1 (cluster of differentiation 213A1), is a human gene. [5] The protein encoded by this gene is a subunit of the interleukin 13 receptor. This subunit forms a receptor complex with IL4 receptor alpha, a subunit shared by IL13 and IL4 receptors.
Pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α also trigger pathological pain. [1] While IL-1β is released by monocytes and macrophages, it is also present in nociceptive DRG neurons. IL-6 plays a role in neuronal reaction to an injury. TNF-α is a well known proinflammatory cytokine present in neurons and the glia.
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Besides IL-22, Th22 cells also produce other cytokines, such as interleukin-13 and tumor necrosis factor alpha , but in very small quantities. [3] Additionally, they could be characterized by their cell surface expression of CD3 , CD4 , CD28 , number of chemokine receptors CCR10 , CCR6 , CCR4 that are associated with cutaneous T cell homing ...
The HuffPost/Chronicle analysis found that subsidization rates tend to be highest at colleges where ticket sales and other revenue is the lowest — meaning that students who have the least interest in their college’s sports teams are often required to pay the most to support them.