Inflammation-induced CD69+ Kupffer cell feedback inhibits T cell proliferation via membrane-bound TGF-β1

Zhang, Xiang; Jiang, Zhengping; Gu, Yan; Liu, Yanfang; Cao, Xuetao; Yun, Han

doi:10.1007/s11427-016-0357-1

Cited by 7 publications

(4 citation statements)

References 61 publications

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“…In addition, TGF-β1 has a negative regulatory role in the immune function of mice. The results of the present study are similar to those reported previously (59). IL-17A is a recognized inflammatory factor, and there was no significance difference in IL-17A levels among the groups.…”

Section: Discussionsupporting

confidence: 92%

Immune promotive effect of bioactive peptides may be mediated by regulating the expression of SOCS1/miR‑155

Chen

2019

Exp Ther Med

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The present study was designed to evaluate the effect of bioactive hepatic peptide (BHP) on the immune function of mice and to examine the mechanism mediated by the related factors cytokine suppressor of cytokine signaling 1 (SOCS1) and microRNA (miR)-155. The mice were divided into eight groups, including a normal mouse group, normal peptide groups (low-dose, mid-dose and high-dose), an immunosuppressed group, and immunosuppressed with peptide groups (low-dose, mid-dose and high-dose). The proliferative ability of splenic lymphocytes was determined in vitro using a Cell Counting kit-8 assay. Wright's staining was used to assess the phagocytic function of macrophages. Histological changes in the spleen were evaluated by hematoxylin-eosin staining. The relevant factors SOCS1/miR-155 were assessed by immunohistochemistry and reverse transcription fluorescence-quantitative polymerase chain reaction analysis. The levels of the cytokines TGF-β1, IL-10 and IL-17A were determined by enzyme-linked immunosorbent assay. First, the organ index, percentage of lymphocytes, phagocytosis experiments and splenic lymphocyte proliferation test results revealed that the immunodeficient mouse model had been successfully established. Second, compared with the control mice, the normal peptide group mice exhibited increased spleen and thymus indices, percentages of lymphocyte subsets, macrophage phagocytosis percentages, phagocytic indices, splenic lymphocyte proliferation and expression of miR-155; however, the expression of SOCS1 was decreased in the normal peptide groups to varying extents. In addition, the expression of SOCS1 was upregulated, whereas that of miR-155 was downregulated in the immunosuppressed group. Compared with the mice in the immunosuppressed group, the mice in the immunosuppressed with peptide groups had increased spleen and thymus indices, percentages of lymphocyte subsets, macrophage phagocytosis percentages, phagocytic indices, splenic lymphocyte proliferation and expression of miR-155; however, the expression of SOCS1 was decreased in the immunosuppressed with peptide groups to varying extents. Following treatment with BHP, the secretion of TGF-β1 in the spleen of the normal mice and immunosuppressed mice was significantly decreased, and the secretion of IL-10 was significantly increased. No significant difference in the expression of IL-17A was observed among the groups. In summary, BHP improved the immune function of the normal mice and immunosuppressed mice. This data provides a scientific basis for the development of bioactive peptide health products.

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Section: Discussionsupporting

confidence: 92%

Immune promotive effect of bioactive peptides may be mediated by regulating the expression of SOCS1/miR‑155

Chen

2019

Exp Ther Med

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“…As expected, only mitotane alone or combined with EF24 decreased the reactivity of Erk1/2 and Akt. Of note, phospho-NF-κB was augmented by EF24 at 5 h in both cell lines and at 72 h in H295R cells (Figure 7A,B); similar results have already been reported, underlining that small doses of curcumin could enhance proliferation and survival [23,24] and could possibly potentiate cell death by DNA damage or oxidative stress [25,26,27]. On the same line, we showed an increase in phosphorylation of Erk1/2 at 5 h in SW13 cells (by EF24 alone or combined), suggesting that under certain circumstances, Erk1/2 can have pro-apoptotic functions, as it is the most important balance between pro- and anti-proliferative signals (Figure 3 and Figure S1), which was already reported by Thomas et al in 2010, where EF24 was shown to significantly induce the upregulation of Erk1/2, JNK, and p38 (MAPK pathway) [20,28,29].…”

Section: Discussionsupporting

confidence: 82%

Biological Effects of EF24, a Curcumin Derivative, Alone or Combined with Mitotane in Adrenocortical Tumor Cell Lines

et al. 2019

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Background: Curcumin has numerous properties and is used in many preclinical conditions, including cancer. It has low bioavailability, while its derivative EF24 shows enhanced solubility. However, its effects have never been explored in adrenocortical tumor cell models. The efficacy of EF24 alone or combined with mitotane (reference drug for adrenocortical cancer) was evaluated in two adrenocortical tumor cell lines, SW13 and H295R. Method and Results: EF24 reduced cell viability with an IC50 (half maximal inhibitory concentration) of 6.5 ± 2.4 μM and 4.9 ± 2.8 μM for SW13 and H295R cells, respectively. Combination index (EF24 associated with mitotane) suggested an additivity effect in both cell lines. Cell cycle analysis revealed an increase in subG0/G1 phase, while motility assay showed a decrease in migratory cell capacity, and similarly, clonogenic assay indicated that EF24 could reduce colony numbers. Furthermore, Wnt/β-catenin, NF-κB, MAPK, and PI3k/Akt pathways were modulated by Western blot analysis when treating cells with EF24 alone or combined with mitotane. In addition, intracellular reactive oxygen species levels increased in both cell lines. Conclusion: This work analyzed EF24 in adrenocortical tumor cell lines for the first time. These results suggest that EF24 could potentially impact on adrenocortical tumors, laying the foundation for further research in animal models.

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“…The positive correlation between C1QA and CD68 and the negative relationship between MARCKSL1 and N4BP2L2 are novel findings in STAD research. In lung cancer, CD68 has been associated with tumour‐associated macrophages and linked to poor prognosis, 34 but its relationship with C1QA in STAD suggests a unique immune modulation. Comparatively, the negative interaction of MARCKSL1 and N4BP2L2 is a relatively unexplored area and could be pivotal in understanding the immune evasion mechanisms in STAD.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Differential genetic mutations and immune cell infiltration in high‐ and low‐risk STAD: Implications for prognosis and immunotherapy efficacy

Deng,

Sun,

et al. 2024

J Cellular Molecular Medi

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This study investigates genetic mutations and immune cell dynamics in stomach adenocarcinoma (STAD), focusing on identifying prognostic markers and therapeutic targets. Analysis of TCGA‐STAD samples revealed C > A as the most common single nucleotide variant (SNV) in both high and low‐risk groups. Key mutated driver genes included TTN, TP53 and MUC16, with frame‐shift mutations more prevalent in the low‐risk group and missense mutations in the high‐risk group. Interaction analysis of hub genes such as C1QA and CD68 showed significant correlations, impacting immune cell infiltration patterns. Using ssGSEA, we found higher immune cell infiltration (B cells, CD4+ T cells, CD8+ T cells, DC cells, NK cells) in the high‐risk group, correlated with increased risk scores. xCell algorithm results indicated distinct immune infiltration levels between the groups. The study's risk scoring model proved effective in prognosis prediction and immunotherapy efficacy assessment. Key molecules like CD28, CD27 and SLAMF7 correlated significantly with risk scores, suggesting potential targets for high‐risk STAD patients. Drug sensitivity analysis showed a negative correlation between risk scores and sensitivity to certain treatments, indicating potential therapeutic options for high‐risk STAD patients. We also validated the carcinogenic role of RPL14 in gastric cancer through phenotypic experiments, demonstrating its influence on cancer cell proliferation, invasion and migration. Overall, this research provides crucial insights into the genetic and immune aspects of STAD, highlighting the importance of a risk scoring model for personalized treatment strategies and clinical decision‐making in gastric cancer management.

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Inflammation-induced CD69+ Kupffer cell feedback inhibits T cell proliferation via membrane-bound TGF-β1

Cited by 7 publications

References 61 publications

Immune promotive effect of bioactive peptides may be mediated by regulating the expression of SOCS1/miR‑155

Immune promotive effect of bioactive peptides may be mediated by regulating the expression of SOCS1/miR‑155

Biological Effects of EF24, a Curcumin Derivative, Alone or Combined with Mitotane in Adrenocortical Tumor Cell Lines

RETRACTED: Differential genetic mutations and immune cell infiltration in high‐ and low‐risk STAD: Implications for prognosis and immunotherapy efficacy

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