◀ Back to IL13
IL13 — MYD88
Text-mined interactions from Literome
Oshikawa et al., Biochem Biophys Res Commun 2003
(Lung Diseases) :
The results demonstrated three patterns of gene expression : the TLR2 and myeloid differentiation factor 88 (
MyD88 ) gene expressions were induced in AM in
response to lipopolysaccharide (LPS),
interleukin (IL)-1beta , or tumor necrosis factor-alpha or in the lung tissue of an LPS induced acute lung injury model ; the gene expressions of TLR1, -3, -6, CD14, and MD2 were unchanged ; and the TLR4 and TLR5 gene expressions were downregulated in AM following inflammatory stimuli
Rad et al., Gastroenterology 2007
(Gastritis...) :
The adaptor protein
Myd88 mediates Toll-like receptor ( TLR ),
interleukin (IL)-1 , and IL-18 signaling
Leichtle et al., BMC immunology 2009
(Otitis Media) :
Activated TLRs signal via two alternative intracellular signaling molecules with differing effects ;
MyD88 ( Myeloid differentiation primary response gene 88 )
inducing primarily
interleukin expression and TRIF ( Tir-domain containing adaptor inducing interferon beta ) mediating type I interferon ( IFN ) expression
Kissner et al., Innate Immun 2011
(Disease Models, Animal...) :
Our results indicated that elevated tumor necrosis factor-a, interferon-?,
interleukin (IL)-1a/ß and IL-6 production from mouse spleen cells treated with SEB alone or in combination with lipopolysaccharide (LPS) was
regulated by
MyD88
Jobbings et al., PloS one 2013
(Listeriosis) :
Osteopontin, IL-2, IL-4,
IL-13 and granulocyte macrophage colony stimulating factor ( GM-CSF ), and chemokines including CCL2, CCL3, CCL4 and CCL5 are released in a
MyD88 dependent manner