Search

N6‐methyladenosine (m6A) RNA methylation is a reversible posttranscriptional modification in eukaryotes involving three types of functional proteins: "writers", "erasers", and "readers". m6A regulates the metabolism of messenger RNAs and noncoding RNAs through RNA structure, splicing, stability, export, and translation, thereby participating in various physiological and pathological processes. Here, we summarize the current state of m6A methylation researches, focusing on how these modifications modulate the fate decisions of innate and adaptive immune cells and regulate immune responses in immune‐associated diseases, including viral infections and cancer. These studies showed that m6A modifications and m6A modifying proteins play a critical role in pathogen recognition, immune cell activation, immune cell fate decisions, and immune reactions. m6A is a novel regulator of immune system homeostasis and activation. [ABSTRACT FROM AUTHOR]

The gut of mammals is considered as a harmonious ecosystem mediated by intestinal microbiota and the host. Both bacteria and mammalian immune cells show region‐related distribution characteristics, and the interaction between the two could be demonstrated by synergetic roles in maintaining intestinal homeostasis and dysregulation in intestinal inflammation. The harmonious interplay between bacteria and host requires fine‐tuned regulations by environmental and genetic factors. Thus, the disturbed immune response to microbial components or metabolites and dysbiosis related to immunodeficiency are absolute risk factors to intestinal inflammation and cancer. In this review, we discuss the crosstalk between bacteria and host immunity in the gut and highlight the critical roles of bidirectional regulation between bacteria and the mammalian immune system involved in intestinal inflammation. [ABSTRACT FROM AUTHOR]

The mammalian target of rapamycin (mTOR) is an evolutionarily conserved serine/threonine kinase which has a central role in the regulation of cell growth and metabolism. In the study of the mTOR signaling pathway, tuberous sclerosis complex (TSC) 1/2 complex is identified as a critical regulator of mTOR activity. TSC1/2 plays important roles for immune cell homeostasis and differentiation by negative control of mTOR signaling pathway. TSC1/2-mTOR pathway is proving to be a central point in regulating immune function of diverse immune cells. In this review, we discuss the function of TSC1/2-mTOR to direct the innate and adaptive immune cell development and function. Furthermore, we focus on the role of TSC1/2-mTOR signaling pathway in immune cell mediated diseases, especially autoimmunity. J. Cell. Physiol. 229: 17-26, 2014. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Macrophages are central mediators of the immune, contributing both to the initiation and the resolution of inflammation. The concept of macrophage activation and program has stimulated interest in its definition, and functional significance in homeostasis and diseases. It has been known that macrophages could be differently activated and programmed into different functional subtypes in response to different types of antigen stumuli or different kinds of cytokines present in the microenvironment and could thus profoundly influence immune responses, but little is known about the state and exact regulatory mechanism of macrophage activation and program from cell or molecular signaling level in immunity. In this review, we summarize the recent finding regarding the regulatory mechanism of macrophage activation and program toward M1 and M2, especially on M2 macrophages. J. Cell. Physiol. 228: 502-512, 2013. © 2012 Wiley Periodicals, Inc. [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]

N 6 -methyladenosine (m 6 A) RNA methylation is a reversible posttranscriptional modification in eukaryotes involving three types of functional proteins: "writers", "erasers", and "readers". m 6 A regulates the metabolism of messenger RNAs and noncoding RNAs through RNA structure, splicing, stability, export, and translation, thereby participating in various physiological and pathological processes. Here, we summarize the current state of m 6 A methylation researches, focusing on how these modifications modulate the fate decisions of innate and adaptive immune cells and regulate immune responses in immune-associated diseases, including viral infections and cancer. These studies showed that m 6 A modifications and m 6 A modifying proteins play a critical role in pathogen recognition, immune cell activation, immune cell fate decisions, and immune reactions. m 6 A is a novel regulator of immune system homeostasis and activation., (© 2021 Wiley Periodicals LLC.)