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  • In this review we aim to


    In this review, we aim to provide a comprehensive understanding of: 1) how AT-resident CD4+ T cell subpopulations regulate the metabolic status of AT; and 2) how adipocytes as antigen presenting cells to modulate the activities of CD4+ T cell subpopulations in AT.
    Under condition with obesity, adipose CD4+ T cells are activated or decreased to maintain the pro-inflammatory state. Adipocytes have been found to act as antigen-presenting cells to regulate CD4+ T cell functions in AT inflammation (Fig. 1B). Adipocyte-produced factors such as adipokines, and adipocyte-derived lipids have shown to modulate CD4+ T cell function [73], [74]. Additionally, adipocytes may activate CD4+ T cells by expressing major histocompatibility complex (MHC) class II and co-stimulatory membrane receptors to regulate adaptive immune responses to AT inflammation [75]. Thus, it would be important to investigate the function of adipocytes as antigen presenting cells in regulating CD4+ T cell activities in AT inflammation.
    Conclusions and future directions In recent years, AT has been considered as a highly active organ, which plays not only metabolic functions, but also endocrine and immune functions in maintaining whole-body energy homeostasis. Accumulating evidence emphasized the roles of AT-resident CD4+ T cells in the pathogenesis of obesity and obesity-associated diseases. Th1 cells and Th17 cells (pro-inflammatory CD4+ T cells) were accumulated, whereas Th2 cells and Treg cells (anti-inflammatory CD4+ T cells) were reduced in AT during the progression of obesity and obesity-associated disorders. Although evidence provided promising perspectives for the development of obesity and related disorders therapies using CD4+ T cells as a drug target, several questions still needed to be addressed. For example, what are the specific AT-restricted Decoquinate responsible for the population alterations of different CD4+ T cell subtypes in individuals with obesity? In addition, adipocyte-derived lipids regulate CD4+ T cell proliferation, but what kind of lipids can exert this role and what subtypes of CD4+ T cell can be changed are still unclear. Moreover, whether other adipocyte-derived metabolites regulate CD4+ T cell function needs to be addressed. Better understanding of these questions will further provide insights into AT-resident CD4+ T cell-targeting therapies for treating obesity and obesity-associated metabolic disorders.
    Introduction The majority of cutaneous T cell lymphomas represent either mycosis fungoides (MF) or primary cutaneous CD30 positive lymphoproliferative disorders (LPD) either in the context of anaplastic large cell lymphoma (ALCL) or lymphomatoid papulosis (LYP). The remainder comprises rare forms of cutaneous lymphoma, which cumulatively represent less than 5% of all cutaneous lymphomas. These less common variants of cutaneous T cell lymphoma encompass a broad clinical and morphologic spectrum ranging from certain low grade lymphoid neoplasms that have now been recategorized as lymphoproliferative disorders such as so called primary cutaneous CD4+ small/medium sized pleomorphic T cell LPD and CD8+ indolent lymphoid proliferation of the face and acral sites to those lymphomas that exhibit an aggressive clinical course. This latter category includes primary cutaneous gamma delta T cell lymphoma, CD30 negative large cell T cell lymphoma, primary cutaneous aggressive epidermotropic CD8+ T cell lymphoma, and NK-T cell lymphoma [[1], [2], [3]]. The therapeutic approaches are as varied as the nosologic classification ranging from topical therapy for early stage MF to aggressive ablative chemotherapy with stem cell transplantation in certain forms of aggressive peripheral T cell lymphoma [4]. T cells exhibit a dynamic phenotype and function that evolves with age, attributable to the repetitive antigenic exposure that occurs through life. A pathological acceleration of immunosenescence occurs in the setting of autoimmune diseases or chronic viral infections due to the extent of adaptive immune responses triggered by response provoking antigens. Each effective immune response to the cognate antigen induces progressive cell differentiation with resultant restriction of the T cell repertoire and ultimately cell cycle arrest. The latter is attributable to critical telomere length reduction inducing a state of replicative senescence. Although these T cells are senescent, they acquire new functional capabilities such as the expression of cytotoxic proteins [[5], [6], [7]].