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IL28A encodes a cytokine distantly related to type I interferons and the IL-10 family.
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IFN-lambda2 and its receptor may become targets of anti-cancer therapy.
IL28 controls proliferation of IECs in mice with colitis and accelerates mucosal healing by activating STAT1 (show STAT1 Antibodies).
IL-28A is capable of exacerbating a T-cell-mediated autoimmune disease.
Data indicate that rotavirus infection induces production of interferon (show IFNA Antibodies)-lambda (IFN-lambda) and interleukin 22 (IL-22 (show IL22 Antibodies)) by intestinal epithelial cells.
IL-28A exerts its antiinflammatory effect by restricting recruitment of IL-1b (show IL1B Antibodies)-expressing neutrophils
The level of IFN-lambda2 was significantly increased in the infected cells treated with with shRNAs against influenza a virus M1.
IFN-lambda2 limits VSV replication in the mouse lung.
Data indicate that IPS-1 (show ISYNA1 Antibodies)-dependent pathway plays a crucial role in type III IFN production by CD8 (show CD8A Antibodies)(+) dendritic cells (DCs) and hepatocytes in response to hepatitis C virus (HCV), leading to cytoplasmic antiviral protein expressions.
NS of severe fever with thrombocytopenia syndrome virus inhibited the activity of IFN-alpha1 (show IFNA1 Antibodies), IFN-beta (show IFNB1 Antibodies), IFN-lambda1 and IFN-lambda2 through inhibition of STAT1 (show STAT1 Antibodies) phosphorylation.
Studies indicate that the type III interferons (IFNs) or IFN-lambdas consists of four members: IFN-lambda1 (IL-29 (show IL29 Antibodies)), IFN-lambda2 (IL28A), IFN-lambda3 (IL-28B (show IL28B Antibodies)) and IFN-lambda4.
Results showed no association between genotypes and alleles of IL28A, IL28B (show IL28B Antibodies) or IL29 (show IL29 Antibodies) polymorphisms and Hepatitis C virus infection.
this study provides evidence for potential IL-28A participation in Behcet's diseaseand its value as a therapeutic agent.
Interferon (show IFNA Antibodies) regulatory factor (IRF)-3 (show IRF3 Antibodies) and -7 are the key transcriptional factors for the induction of IL-28A and IL-28B (show IL28B Antibodies) genes, whereas NF-kappaB (show NFKB1 Antibodies) is an additional requirement for the induction of the IL-29 (show IL29 Antibodies) gene.
The results show that IL-28A/IL-28AR1 dyad-induced wound healing migration requires NF-kappaB (show NFKB1 Antibodies)-mediated MMP-9 (show MMP9 Antibodies) expression by MAPK (show MAPK1 Antibodies) activation.
IL-28 genotype was not associated with response to interferon (show IFNA Antibodies) treatment (OR for GT/GG vs. TT, 0.881 (95%CI 0.388 - 2.002); P = 0.762; OR for CT/CC vs. TT, 0.902 (95%CI 0.458 - 1.778); P = 0.766).
p38 MAPK (show MAPK14 Antibodies) pathway mediates IL-28A-induced cell migration through MMP-9 (show MMP9 Antibodies) expression by activating NF-kappaB (show NFKB1 Antibodies) and AP-1 (show FOSB Antibodies) binding motifs.
Elevated expression of inflammatory cytokines (IL-5 (show IL5 Antibodies), IL-20 (show IL20 Antibodies), and IL-28A) is associated with bladder cancer development.
Plasmacytoid dendritic cells are major producers of IFN-lambda2 (a type III interferon (show IFNA Antibodies)) in response to viral stimulation.
Cytokine with immunomodulatory activity. Up-regulates MHC class I antigen expression. Displays potent antiviral activity. Also displays antitumor activity. Ligand for the heterodimeric class II cytokine receptor composed of IL10RB and IL28RA. The ligand/receptor complex seems to signal through the Jak-STAT pathway.
, interferon lambda-2
, interleukin 28A
, cytokine Zcyto20
, interferon lambda 2
, interferon-lambda 2
, interleukin 28A (interferon, lambda 2)