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#28096407   2017/01/18 Save this To Up

Development of chronic allergic responses by dampening Bcl6-mediated suppressor activity in memory T helper 2 cells.

Mice deficient in the transcriptional repressor B-cell CLL/lymphoma 6 (Bcl6) exhibit similar T helper 2 (TH2) immune responses as patients with allergic diseases. However, the molecular mechanisms underlying Bcl6-directed regulation of TH2 cytokine genes remain unclear. We identified multiple Bcl6/STAT binding sites (BSs) in TH2 cytokine gene loci. We found that Bcl6 is modestly associated with the BSs, and it had no significant effect on cytokine production in newly differentiated TH2 cells. Contrarily, in memory TH2 (mTH2) cells derived from adaptively transferred TH2 effectors, Bcl6 outcompeted STAT5 for binding to TH2 cytokine gene loci, particularly Interleukin4 (Il4) loci, and attenuated GATA binding protein 3 (GATA3) binding to highly conserved intron enhancer regions in mTH2 cells. Bcl6 suppressed cytokine production epigenetically in mTH2 cells to negatively tune histone acetylation at TH2 cytokine gene loci, including Il4 loci. In addition, IL-33, a pro-TH2 cytokine, diminished Bcl6's association with loci to which GATA3 recruitment was inversely augmented, resulting in altered IL-4, but not IL-5 and IL-13, production in mTH2 cells but no altered production in newly differentiated TH2 cells. Use of a murine asthma model that generates high levels of pro-TH2 cytokines, such as IL-33, suggested that the suppressive function of Bcl6 in mTH2 cells is abolished in severe asthma. These findings indicate a role of the interaction between TH2-promoting factors and Bcl6 in promoting appropriate IL-4 production in mTH2 cells and suggest that chronic allergic diseases involve the TH2-promoting factor-mediated functional breakdown of Bcl6, resulting in allergy exacerbation.

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#27840912   2016/11/14 Save this To Up

Aberrant expression of B7‑H4 may contribute to the development of hepatocellular carcinoma.

In order to determine the effect of B7‑H4 on the development of human hepatocellular carcinoma (HCC), the expression levels of B7‑H4 were evaluated using reverse transcription‑polymerase chain reaction and flow cytometry in HL‑7702 and Huh7 cells. B7‑H4 protein expression levels were analyzed using western blotting and immunohistochemistry in HCC tissues collected from patients and from a mouse tumor model. Soluble B7‑H4 (sB7‑H4), interferon‑γ (IFN‑γ), and interleukin‑4 (IL‑4) in blood serum were assessed using ELISA in patients with HCC and mice injected with tumor cells. B7‑H4 was expressed in HCC cell lines, mouse tumor tissues and HCC patient tissues. However, B7‑H4 was not detected in HL‑7702 cells or normal human liver tissues. The expression level of B7‑H4 was positively correlated with tumor‑node‑metastasis (TNM) stage, lymph node metastasis, and differentiation degree in patients with HCC. sB7‑H4 levels in blood serum samples collected from patients with HCC and tumorigenic mice were higher compared with healthy controls. Expression levels of IFN‑γ were reduced, and IL‑4 levels were increased in blood serum samples of patients with HCC and tumorigenic mice compared with healthy controls. sB7‑H4 expression levels were negatively correlated with IFN‑γ levels, and with the ratio of IFN‑γ to IL‑4. Additionally, sB7‑H4 was positively correlated with IL‑4 levels in mouse tumor tissues, serum samples obtained from tumorigenic mice and human HCC patients. Notably, the levels of sB7‑H4 and IL‑4 were positively correlated and IFN‑γ was negatively correlated with the TNM stage of patients with HCC. In addition, sB7‑H4 and IL‑4 expression levels increased and levels of IFN‑γ and the ratio of IFN‑γ/IL‑4 decreased as a function of time post tumor implantation in the mouse model. The present study determined that aberrant expression of B7‑H4 contributed to HCC development. B7‑H4 may be a potential target for therapy and diagnosis of HCC.

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#25650554   2015/03/17 Save this To Up

Role of the complement anaphylatoxin C5a-receptor pathway in atopic dermatitis in mice.

Atopic dermatitis (AD) is a chronic inflammatory skin disease with a genetic background. The C5a‑receptor (C5aR) pathway has been reported to be involved in AD; however, the precise pathogenesis remains to be elucidated. In the present study, the contribution of the C5aR pathway to AD in mice was investigated. A BALB/c mouse model of AD was induced by application of 2,4‑dinitrochlorobenzene (DNCB) onto hairless dorsal skin. Following DNCB application for 2 weeks, C5aR expression in skin tissue was assessed by reverse transcription quantitative polymerase chain reaction. C5aR expression in skin tissue was significantly increased in mice with AD. In an additional experiment, C5aR antagonist (C5aRA) intracutaneously injected in combination with DNCB treatment. The skin‑fold thickness, number of total infiltrating leukocytes and mast cells infiltrating in skin tissue were measured. Interleukin‑4 (IL‑4) and interferon‑γ (IFN‑γ) levels in skin tissue and IL‑4, IFN‑γ, histamine and immunoglobulin E (IgE) levels in serum were measured using ELISA. The skin‑fold thickness, numbers of total infiltrating leukocytes and mast cells in skin tissue, as well as levels of IL‑4, IFN‑γ, histamine and IgE were significantly increased in mice with AD. However, simultaneous treatment with C5aRA significantly attenuated increases in skin fold thickness and the numbers of total infiltrating leukocytes and mast cells in skin tissue. Treatment with C5aRA also decreased IL‑4 and IFN‑γ levels in skin tissue, as well as the levels of IL‑4, IFN‑γ, histamine and IgE in the serum. In conclusion, C5aRA inhibited AD in mice, possibly through suppression of the C5aR‑mediated cascade action of mast cells.

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