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Acts as a negative regulator of innate and adaptive immunity by maintaining immune homeostasis.
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The expression of TIPE2 in THP1 (show GLI2 Antibodies) cells may be upregulated by Poly I:C.
In conclusion, for the first time, we discovered that the Th2 milieu is able to upregulate TIPE2 expression in macrophages, which facilitates the change in macrophage phenotype and function and, in turn, potentially exaggerates eosinophilic inflammation and disease progression in chronic rhinosinusitis with nasal polyps.
TIPE2 may participate in T2DM by regulating TNF-alpha (show TNF Antibodies) production
Our study identifies the molecular mechanisms underlying the interplay of TNF-alpha (show TNF Antibodies), TIPE2, and apoptosis during allograft rejection, and it suggests that both TNF-alpha (show TNF Antibodies) and TIPE2 might be potential targets for the successfully grafted corneal endothelium.
TIPE2 inhibited the expression of asthma-related inflammatory factors in hyperstretched BEAS-2B cells by suppressing the Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling pathway.
TIPE2 might be associated with immune clearance of patients with chronic hepatitis B.
TIPE2 could play important roles in maintaining the maternal-fetal tolerance and decreased TIPE2 expression in the decidua may be related to the development of missed abortion.
TIPE2 suppressed tumor invasiveness and angiogenesis in non-small cell lung cancer via inhibiting the activation of Rac1 and subsequently weakening its downstream effects, including F-actin polymerization and VEGF (show VEGFA Antibodies) expression.
the expression of TIPE2 protein could be a predictor of better prognosis for DLBCL.
Insufficient expression of TIPE2 might be involved in the hyperreactivity of monocyte to Toll (show TLR4 Antibodies)-like receptor ligands in primary biliary cirrhosis.
the enhancement of stat3 (show STAT3 Antibodies) phosphorylation and decrease of LPS (show TLR4 Antibodies)-induced p65 (show NFkBP65 Antibodies) translocation were achieved by nicotine treatment..this study revealed that TIPE2 upregulation and stat3 (show STAT3 Antibodies) phosphorylation contribute to nicotine-mediated anti-inflammation effect, indicating that TIPE2 and stat3 (show STAT3 Antibodies) might be potential molecules for dealing with inflammation-associated diseases.
TIPE-2 held a protective effect on liver fibrosis and could be a potential therapeutic target.
Results suggest that tumor necrosis factor alpha-induced protein 8-like 2 (TIPE2) appeared to be a critical immunoregulatory molecule which affected dendritic cells (DCs) maturation and subsequent T-cell mediated immunity.
The results reported here indicated a crucial role for TIPE2 in the infiltration of leukocytes into neural tissue in Experimental Autoimmune Encephalomyelitis.
TIPE2 inhibited breast cancer development and metastasis possibly via promoting CD8 (show CD8A Antibodies)(+) T and NK cell-mediated antitumor immune responses
Our current study shows that TIPE2-deficient bone-marrow cells are defective in IL-4 (show IL4 Antibodies) induced M2 macrophage differentiation in vitro. TIPE2 promotes phosphoinositide metabolism and the activation of the down-stream AKT (show AKT1 Antibodies) signaling pathway, which in turn leads to the expression of markers specific for M2 macrophages.
The present study demonstrates that TIPE2 acts as a novel negative regulator of inflammatory and immune responses through TAK1 (show NR2C2 Antibodies) signaling.
Data show that after tumor necrosis factor alpha-induced protein 8 like-2 (TIPE2) gene was down-regulated, the expression of the CD69 antigen (show CD69 Antibodies) was increased, and the proliferation of T lymphocytes and the secretion of cytokines IL-2 (show IL2 Antibodies) and IFN-gamma (show IFNG Antibodies) were enhanced.
TIPE2 alleviates experimental SLE through induction of macrophage polarization to a M2 phenotype, which may be used as a promising therapeutic strategy for treating SLE.
Acts as a negative regulator of innate and adaptive immunity by maintaining immune homeostasis. Negative regulator of Toll-like receptor and T-cell receptor function. Prevents hyperresponsiveness of the immune system and maintains immune homeostasis. Inhibits jun/ap1 and NF-kappa-B activation. Promotes Fas-induced apoptosis (By similarity).
TNF alpha-induced protein 8-like protein 2
, TNFAIP8-like protein 2
, inflammation factor 20
, inflammation factor protein 20
, tumor necrosis factor alpha-induced protein 8-like protein 2
, tumor necrosis factor, alpha-induced protein 8-like protein 2
, Tumor necrosis factor, alpha-induced protein 8-like protein 2
, tumor necrosis factor, alpha-induced protein 8-like protein 2 a