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transcription tipping points for t follicular helper cell and t-helper 1 cell fate commitment

Cellular & Molecular Immunology 2021年第3期18卷 528-538页

作者： Amania A.Sheikh Joanna R.Groom Divisions of Immunology and Molecular Immunology Walter and Eliza Hall Institute of Medical ResearchParkvilleVIC 3052Australia Department of Medical Biology University of MelbourneParkvilleVIC 3010Australia

During viral infection,immune cells coordinate the induction of inflammatory responses that clear infection and humoral responses that promote protection.CD4^(+)t-cell differentiation sits at the center of this axis.Differentiation toward t-helper 1(th1)cells mediates inflammation and pathogen clearance,while t follicular helper(tfh)cells facilitate germinal center(GC)reactions for the generation of high-affinity antibodies and immune memory.While th1 and tfh differentiation occurs in parallel,these CD4^(+)t-cell identities are mutually exclusive,and progression toward these ends is determined via the upregulation of t-bet and Bcl6,respectively.these lineage-defining transcription factors act in concert with multiple networks of transcriptional regulators that tip the t-bet and Bd6 axis in CD4^(+)t-cell progenitors to either a th1 or tfh fate.It is now clear that these transcriptional networks are guided by cytokine cues that are not only varied between distinct viral infections but also dynamically altered throughout the duration of infection.thus,multiple intrinsic and extrinsic factors combine to specify the fate,plasticity,and function of th1 and tfh cells during infection.Here,we review the current information on the mode of action of the lineage-defining transcription factors Bcl6 and t-bet and how they act individually and in complex to govern CD4^(+)t-cell ontogeny.Furthermore,we outline the multifaceted transcriptional regulatory networks that act upstream and downstream of Bcl6 and t-bet to tip the differentiation equilibrium toward either a tfh or th1 fate and how these are impacted by dynamic inflammatory cues.

关键词： Cytokines Infection t follicular helper cells t-helper 1 cells transcription factors

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Serum soluble suppression of tumorigenicity 2 as a novel inflammatory marker predicts the severity of acute pancreatitis

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World Journal of Gastroenterology 2021年第38期27卷 6489-6500页

作者： Yan Zhang Bo Cheng Zhong-Wei Wu Zong-Chao Cui Yao-Dong Song San-Yang Chen Yan-Na Liu Chang-Ju Zhu Department of Emergency the First Affiliated Hospital of Zhengzhou UniversityZhengzhou 450052Henan ProvinceChina

BACKGROUND Acute pancreatitis(AP)is an inflammatory disease in which the regulatory pathway is complex and not well understood.Soluble suppression of tumorigenicity 2(sSt2)protein receptor functions as a decoy receptor for interleukin(IL)-33 to prevent IL-33/suppression of tumorigenicity 2L(St2L)-pathwaymediated t helper(th)2 immune responses.AIM to investigate the role of sSt2 in AP.MEtHODS We assessed the association between sSt2 and severity of AP in 123 patients enrolled in this study.the serum levels of sSt2,C-reactive protein(CRP)and th1-and th2-related cytokines,including interferon(IFN)-γ,tumor necrosis factor(tNF)-α,IL-2,IL-4,IL-5 and IL-13,were measured by highly sensitive ELISA,and the severity of AP in patients was evaluated by the 2012 Atlanta Classification Criteria.RESULtS Serum sSt2 levels were significantly increased in AP patients,and further,these levels were significantly elevated in severe AP(SAP)patients compared to moderately severe AP(MSAP)and mild AP(MAP)patients.Logistic regression showed sSt2 was a predictor of SAP[odds ratio(OR):1.003(1.001–1.006),P=0.000].sSt2 cutoff point was 1190 pg/mL,and sSt2 above this cutoff was associated with SAP.sSt2 was also a predictor of any organ failure and mortality during AP[OR:1.006(1.003–1.009),P=0.000,OR:1.002(1.001–1.004),P=0.012,respectively].Additionally,the th1-related cytokines IFN-γand tNF-αin the SAP group were higher and the th2-related cytokine IL-4 in the SAP group was significantly lower than those in MSAP and MAP groups.CONCLUSION sSt2 may be used as a novel inflammatory marker in predicting AP severity and may regulate the function and differentiation of IL-33/St2-mediated th1 and th2 Lymphocytes in AP homeostasis.

关键词： Acute pancreatitis Soluble suppression of tumorigenicity 2 t-helper 1 cells t-helper 2 cells Interleukin-33 Biomarker

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