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Neutrophil extracellular trap (NET) is one of the defense functions of neutrophils, which has a rapid ability to kill infections and is also crucial in a variety of immune-associated diseases including infections, tumors and autoimmune diseases. Recent studies have shown that NETs are closely related to the development of tumors. The regulatory role of NETs in tumors has been of interest to researchers. In addition to awakening latent tumor cells, NETs can also promote the proliferation and development of tumor cells and their metastasis to other sites. At the same time, NETs also have the effect of inhibiting tumors. At present, there are some new advances in the impact of NETs on tumor development, which will provide a more theoretical basis for developing NET-targeted drugs. Therefore, this review just summarized the formation process of NETs, the regulation of tumor development and the treatment methods based on NETs., (© 2023 UICC.)

Follicular T helper (T FH ) cells are specialized T cells that support B cells, which are essential for humoral immunity. T FH cells express the transcription factor B-cell lymphoma 6 (Bcl-6), chemokine (C-X-C motif) receptor (CXCR) 5, the surface receptors programmed cell death protein 1 (PD-1) and inducible T-cell costimulator (ICOS), the cytokine IL-21 and other molecules. The activation, proliferation and differentiation of T FH cells are closely related to dynamic changes in cellular metabolism. In this review, we summarize the progress made in understanding the development and functional differentiation of T FH cells. Specifically, we focus on the regulatory mechanisms of T FH cell functional differentiation, including regulatory signalling pathways and the metabolic regulatory mechanisms of T FH cells. In addition, T FH cells are closely related to immune-associated diseases, including infections, autoimmune diseases and cancers., (© 2020 John Wiley & Sons Ltd.)

Mammalian STE20-like protein kinases (MST), including MST1, MST2, MST3, and MST4, belong to the germinal center kinase (GCK) family. Kinase MST1/2 is an important component of the Hippo pathway in regulating cell proliferation, tissue homeostasis, and organ development. Recent studies have shown that Hippo kinase MST1/2 plays a crucial role in immune-associated diseases, which has attracted extensive attention of researchers. This review summarizes recent research on Hippo kinases MST1/2 in regulating the function of immune cells in innate and adaptive immune systems, and also includes its regulatory role and significance in cancer, infection, and autoimmune diseases.

Inflammasome activation and subsequent inflammatory cytokine secretion are essential for innate immune defence against multiple stimuli and are regarded as a link to adaptive immune responses. Dysfunction of inflammasome activation has been discovered at the onset or progression of infectious diseases, autoimmune diseases and cancer, all of which are also associated with metabolic factors. Furthermore, many studies concerning the metabolic regulation of inflammasome activation have emerged in recent years, especially regarding the activity of the NLRP3 inflammasome under metabolic reprogramming. In this review, we discuss the molecular mechanisms of the interactions between metabolic pathways and inflammasome activation, which exerts further important effects on various diseases., (© 2019 John Wiley & Sons Ltd.)

Naïve CD4+T cells differentiate into various T cell subsets depending on the specific cytokine environment. TH9 cells are less well-characterized than other T cell subsets, and factors that control their development and function have only recently been identified. It is now clear that TH9 cells play critical roles in immune-mediated diseases, including allergic airway, autoimmune and inflammatory bowel diseases, and cancer. Thus, the promotion or suppression of TH9 cell differentiation, transcriptional control and function may provide novel treatments for clinical inflammation, autoimmune diseases and tumors.

Myeloid-derived suppressor cells (MDSCs) play a critical role in suppressing immune responses in patients with cancer or severe inflammation. Recent studies have focused on the strong relationship between MDSCs and autoimmune diseases, such as autoimmune hepatitis, inflammatory bowel disease and experimental autoimmune encephalomyelitis. Interestingly, MDSCs appear to serve multifaceted functions in autoimmunity, playing both protective and pathogenic roles. Therefore, although MDSCs may be a functional target for the therapy of autoimmune diseases, the disorders that accompany such treatments should be noted. In this manuscript, we summarize the functions and molecular regulation of MDSCs in immunity and autoimmune disease.

Follicular T helper (Tfh) cells play important roles in facilitating B‐cell differentiation and inducing the antibody response in humoral immunity and immune‐associated inflammatory diseases, including infections, autoimmune diseases, and cancers. However, Tfh cell differentiation is mainly achieved through self‐directed differentiation regulation and the indirect regulation mechanism of antigen‐presenting cells (APCs). During the direct intrinsic differentiation of naïve CD4+ T cells into Tfh cells, Bcl‐6, as the characteristic transcription factor, plays the core role of transcriptional regulation. APCs indirectly drive Tfh cell differentiation mainly by changing cytokine secretion mechanisms. Altered metabolic signaling is also critically involved in Tfh cell differentiation. This review summarizes the recent progress in understanding the direct and indirect regulatory signals and metabolic mechanisms of Tfh cell differentiation and function in immune‐associated diseases. [ABSTRACT FROM AUTHOR]

T helper 17 (TH17) cells have well-described roles in autoimmune disease. However, TH17 is not stable in some physiological or pathological courses. Also, TH17 cells can reciprocally modulate and convert into other helper T cell subpopulations. The fully exploring the reciprocal regulatory effects and its immunoregulatory mechanisms are becoming interesting topics in the immunological study. In this review, we summarized reciprocal modulation pattern between TH17 cell and other helper T cell subpopulations in the mouse model of autoimmune diseases and human diseases. J. Cell. Physiol. 226: 8-13, 2010. © 2010 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Regulatory CD4+ CD25+ T (Treg) cells with the ability to suppress host immune responses against self- or non-self antigens play important roles in the processes of autoimmunity, transplant rejection, infectious diseases and cancers. The proper regulation of CD4+ CD25+ Treg cells is thus critical for optimal immune responses. Toll-like receptor (TLR)-mediated recognition of specific structures of invading pathogens initiates innate as well as adaptive immune responses via antigen-presenting cells (APCs). Interestingly, new evidence suggests that TLR signalling may directly or indirectly regulate the immunosuppressive function of CD4+ CD25+ Treg cells in immune responses. TLR signalling may shift the balance between CD4+ T-helper cells and Treg cells, and subsequently influence the outcome of the immune response. This immunomodulation pathway may therefore have potential applications in the treatment of graft rejection, autoimmune diseases, infection diseases and cancers. [ABSTRACT FROM AUTHOR]

Summary: Antigen-presenting cells (APCs) play a crucial role in both innate and adaptive immunity. The mechanisms for APCs to distinguish self and nonself have not been uncovered. In the present manuscript, we hypothesized the balance between the activating and inhibiting receptors on APCs will control the state of APCs. In general, they keep balanced by the endogenous ligands so that APCs are in a non-activating state in the naïve bodies. However, foreign antigens or altered self cells will trigger the activating/inhibiting receptors positively or negatively, so these receptor-mediated signals into APCs will be in tendency to be unbalanced. As long as the activating signals are over the inhibiting receptors, APCs will then be activated to function. This hypothesis will help us to explain how APCs can distinguish self and nonself antigens as well as their close relationships with the occurrence of autoimmune diseases. The activated state of APCs in the early stage of autoimmune diseases may be due to imbalance of the activating/inhibiting receptors on APCs triggered by host endogenous ligands. On the other hand, the poor immunity against tumor cells in the late stage of tumor patients may be partially due to the so-called “tolerance” state of APCs in hosts. We believe that, with the proving by the coming evidences, the impacts of the present hypothesis on basic and clinical immunology would be significant. [Copyright &y& Elsevier]