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Glucose uptake by lymphocytes is dependent on the facilitative glucose transporters (GLUT1, GLUT3, GLUT4, and GLUT6) of the GLUT family and the Na + -coupled glucose transporter SGLT1. GLUTs and SGLTs are widely expressed in mammals, and their expression and functions may affect cell development, homeostasis, activation, and differentiation. This article details the important functions of several GLUTs and SGLTs in lymphocytes and points out that glucose transporters play a key role in supplying energy for lymphocytes, maintaining intracellular glucose homeostasis, and improving the efficiency of immune responses, which reflect their key roles in signal transduction. Probing into the effects of glucose transporters on lymphocyte functions will help to decipher the functioning mechanisms of lymphocytes in diseases. Furthermore, this paper prospects the application values of glucose transporters in lymphocytes from molecular biology, aiming to provide better strategies for the clinical treatment of lymphocyte-related diseases and promote the research and development of targeted therapeutic drugs.

The genesis and progression of cancer is a process of immunoediting that consists of 3 phases, namely elimination, equilibrium and escape phases. This process is also a microevolutionary game process between the body and the tumor. Data from mouse tumors and some human tumors shows that both T cell-based adaptive immunity and innate lymphoid cell (ILC)-based innate immunity participate in cancer immunoediting. The ILCs, which belong to tissue-resident cells and consist of multiple subsets, are a unique branch of the innate immune system discovered over a decade ago. The characteristics and functions of ILCs exhibit significant heterogeneity and are regulated by a variety of factors secreted by various kinds of cells. ILCs participate not only in the regulation of tissue homeostasis and inflammatory responses, but also, through various mechanisms, in the formation of tumor microenvironment and cancer immunoediting process. This paper studies the classification and characteristics of ILCs and their roles and mechanisms in tumors, aiming to explore new thoughts for the pathogenesis, diagnosis and treatment of tumors. [ABSTRACT FROM AUTHOR]

Postmenopausal osteoporosis (PMOP) is a systemic skeletal disorder associated with disturbances in bone metabolism caused by estrogen deficiency during menopause. Major histocompatibility complex class II molecules (MHC-II), central to the protein presentation pathway, are regulated by estrogen and can participate in the adaptive immune response mediated by T and B lymphocytes and promote T cell-derived inflammatory factors, which ultimately promote osteoclast-mediated bone formation and bone resorption in the skeleton. In this paper, to better understand the possible role of MHC-II in postmenopausal osteoporosis, we review estrogen, MHC-II, and lymphocytes, and their potential mechanisms in the differentiation process and functional activity of osteoclasts. [ABSTRACT FROM AUTHOR]

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Copyright of Mycosystema is the property of Mycosystema Editorial Board and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)