Tissue-specific expression of TIPE2 provides insights into its function

Zhang, Guizhong; Hao, Chunyan; Lou, Yunwei; Xi, Wenjin; Wang, Xuping; Wang, Yan; Qu, Zhenzhen; Guo, Chun; Chen, Youhai; Zhang, Yun; Liu, Suxia

doi:10.1016/j.molimm.2010.06.016

Cited by 71 publications

(77 citation statements)

References 17 publications

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“…TIPE1 and TIPE2 appear to be largely inhibitory, that is, they are proapoptotic and anti-proliferative. Unlike TIPE1, 41 TIPE2, which is expressed in mature T cells, 45,46 also has an important role in immune regulation. In contrast, TNFAIP8 and TIPE3 appear to be largely anti-apoptotic, pro-proliferative and pro-migratory.…”

Section: Discussionmentioning

confidence: 99%

“…TIPE2 has been the subject of the most intensive studies to date, perhaps partly due to the initial observation of its preferential lymphoid expression in mice. 45 This observation led to a series of studies that have somewhat elucidated its role in immune system regulation. Despite these studies, the total body of work on all these proteins remains small; based on a PubMed search through 15 June 2016, the number of publications addressing the function of this family of proteins stands as follows: 25, four, 50 and two publications discuss TNFAIP8, TIPE1, TIPE2 and TIPE3, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…18 Follow-up expression studies in mice have found that TIPE2 is preferentially expressed in hematopoietic cells, particularly T cells (including regulatory T cells), 44 whereas it is almost absent from B cells and the B cell zones of lymphoid tissues. 45 In human studies, TIPE2 was found to be much more widely expressed; notably, it was found to be expressed only in differentiated, not progenitor, squamous epithelial cells. 46 TIPE2 has been investigated in the setting of several human diseases.…”

Section: Tipe2 Is a Negative Regulator Of Immunity And Inflammationmentioning

confidence: 99%

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Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Goldsmith

Chen

2017

Cell Mol Immunol

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The TIPE (tumor necrosis factor-α-induced protein 8-like) family are newly described regulators of immunity and tumorigenesis consisting of four highly homologous mammalian proteins: TNFAIP8 (tumor necrosis factor-α-induced protein 8), TIPE1 (TNFAIP8-like 1, or TNFAIP8L1), TIPE2 (TNFAIP8L2) and TIPE3 (TNFAIP8L3). They are the only known transfer proteins of the lipid secondary messengers PIP2 (phosphatidylinositol 4,5-bisphosphate) and PIP3 (phosphatidylinositol 3,4,5-trisphosphate). Cell-surface receptors, such as G-protein-coupled receptors and receptor tyrosine kinases, regulate inflammation and cancer via several signaling pathways, including the nuclear factor (NF)-κB and phosphoinositide-3 kinase (PI3K) pathways, the latter of which is upstream of both Akt and STAT3 activation. An expression analysis in humans demonstrated that the TIPE family is dysregulated in cancer and inflammation, and studies both in mice and in vitro have demonstrated that this family of proteins plays a critical role in tumorigenesis and inflammatory responses. In this review, we summarize the current literature for all four family members, with a special focus on the phenotypic manifestations present in the various knockout murine strains, as well as the related cell signaling that has been elucidated to date.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Tipe2 Is a Negative Regulator Of Immunity And Inflammationmentioning

confidence: 99%

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Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Goldsmith

Chen

2017

Cell Mol Immunol

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“…However, the mechanisms whereby microbes promote them are not well understood. TIPE2, or tumor necrosis factor-α-induced protein 8 (TNFAIP8)-like 2 (TNFAIP8L2), is a member of the TNFAIP8 family, which is preferentially expressed in hematopoietic cells (12)(13)(14)(15)(16)(17)(18). It is significantly down-regulated in patients with infectious or autoimmune disorders (15,19).…”

mentioning

confidence: 99%

TIPE2 protein serves as a negative regulator of phagocytosis and oxidative burst during infection

Wang

Fayngerts

Wang

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

109

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Phagocytosis and oxidative burst are two major effector arms of innate immunity. Although it is known that both are activated by Toll-like receptors (TLRs) and Rac GTPases, how their strengths are controlled in quiescent and TLR-activated cells is not clear. We report here that TIPE2 (TNFAIP8L2) serves as a negative regulator of innate immunity by linking TLRs to Rac. TLRs control the expression levels of TIPE2, which in turn dictates the strengths of phagocytosis and oxidative burst by binding to and blocking Rac GTPases. Consequently, TIPE2 knockout cells have enhanced phagocytic and bactericidal activities and TIPE2 knockout mice are resistant to bacterial infection. Thus, TIPE2 sets the strengths of phagocytosis and oxidative burst and may be targeted to effectively control infections.

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“…As a type of tumor necrosis factor-α-induced protein-8, TIPE2 is primarily expressed by the myeloid and lymphoid immune cells, particularly by T lymphocytes, mononuclear cells and macrophages (17,18). TIPE2 is a negative regulator of inflammation in certain diseases including chronic hepatitis B (19), chronic hepatitis C (20), systemic lupus erythematosus (SLE) (21), diabetic nephropathy (22) and abdominal aortic aneurysm (23), suggesting that it serves an important role in the pathogenesis of inflammatory diseases.…”

Section: Introductionmentioning

confidence: 99%

TIPE2 is negatively correlated with tissue factor and thrombospondin-1 expression in patients with bronchial asthma

et al. 2018

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Abstract. The interaction between inflammatory processes and a hypercoagulant state may aggravate the severity of asthma and stimulate the airway remodeling of asthma. The aim of the current study was to evaluate the association between the negative inflammatory regulator tumor necrosis factor α induced protein-8 like-2 (TIPE2) and the coagulating substances tissue factor (TF) and thrombospondin-1 (TSP-1) in patients with bronchial asthma. Compared with healthy controls, TIPE2 expression was significantly downregulated, whereas TF expression was upregulated in the peripheral blood mononuclear cells (PBMCs) of patients with bronchial asthma. In addition, levels of TF and TSP-1 in the sera were up-regulated in patients with asthma compared with healthy controls. TIPE2 expression was negatively correlated with TF in the PBMCs and sera and was negatively correlated with TSP-1 levels in the sera of patients with bronchial asthma. The results of the current study indicated that anti-inflammatory TIPE2 levels are associated with levels of the coagulation substances TF and TSP-1. However, further studies are required to determine whether TIPE2 participates in the pathogenesis of asthma by interacting with the coagulation substances TF and TSP-1.

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Tissue-specific expression of TIPE2 provides insights into its function

Cited by 71 publications

References 17 publications

Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

Regulation of inflammation and tumorigenesis by the TIPE family of phospholipid transfer proteins

TIPE2 protein serves as a negative regulator of phagocytosis and oxidative burst during infection

TIPE2 is negatively correlated with tissue factor and thrombospondin-1 expression in patients with bronchial asthma

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