Critical Reviews in Immunology最新文献

Triple-negative breast cancer (TNBC) is a type of breast cancer (BC) with high aggressive nature, devoid of receptors for estrogen and progesterone hormones and with overexpression of the HER2/neu protein. It is more aggressive than other types of BC, common occurring in younger women. Recently, preclinical and clinical studies have investigated the use of immune therapies to treat TNBC patients. However, a subset of patients is responding to immunotherapy due to the high level of tumor mutation burden. The bidirectional communication among the tumor microenvironment (TME) cells via signal molecules modulates γδ T cells to support or impair tumor growth. This review emphasizes γδ T cell-mediated immune responses with a special focus on breast cancer. We present the cytotoxic characteristics of γδ T cells. We also present the promising role of γδ T cells in mounting pro-tumor and anti-tumor responses in the TME. Finally, our review focuses on prominent features of γδ T cells as a curse in breast cancer development.

Diabetes mellitus is a class of noncommunicable chronic metabolic disorders marked by hyperglycemia due to insulin production, insulin action or both and has reached epidemic levels around the world. The two most frequent types of diabetes are type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). Despite substantial improvements in the knowledge and treatment of DM, the associated incidence and mortality rates remain steadily increased. Reliable markers for the early detection, monitoring and focused treatment of DM are desperately required. Conversely, microRNAs (miRNAs) have received much significance due to their regulatory involvement in gene expression. Fascinatingly, exosomes can be enclosed into miRNAs to transport or distribute them into the target cells or tissues in which they have a physiological regulatory action. Thus, exosomal miRNAs are proving to be important regulators in the establishment and maintenance of DM, however, further mode of action will be needed to investigate in order to fully comprehend the pathophysiological process. Hereby, this review outlines the recent findings on the role of exosomal miRNAs intending to understand the precise function in diagnostic and therapeutic aspects in T2DM disease.

Gamma delta (γδ) T cells are a subset of T lymphocytes that express T cell receptor γ and 5 chains and display structural and functional heterogeneity. γδ T cells are typically of low abundance in the body and account for 1-5% of the blood lymphocytes and peripheral lymphoid tissues. As a bridge between innate and adaptive immunity, γδ T cells are uniquely poised to rapidly respond to stimulation and can regulate immune responses in peripheral tissues. The dendritic epidermal T cells in the skin epidermis can secrete growth factors to regulate skin homeostasis and re-epithelization and release inflammatory factors to mediate wound healing during skin inflammatory responses. Dermal γδ T cells can regulate the inflammatory process by producing interleukin-17 and other cytokines or chemokines. Here, we offer a review of the immune functions of γδ T cells, intending to understand their role in regulating skin barrier integrity and skin wound healing, which may be crucial for the development of novel therapeutics in skin diseases like atopic dermatitis and psoriasis.

Liquid biopsy is a rapidly evolving diagnostic technique used to analyze tissue-derived information found in the blood or other bodily fluids. It represents a new way to guide therapeutic decisions, mainly in cancer, but its application in other fields of medicine is still growing. Here, we discuss how liquid biopsy has been used in autoimmune rheumatic diseases such as rheumatoid arthritis, systemic lupus erythematosus, or primary Sjögren's syndrome. Additionally, in aspect of liquid biopsy, we analyze the molecular biomarkers utilized in the field of rheumatology, including circulating cell-free DNA, microRNA, and proteomic content.

Idiopathic pulmonary fibrosis (IPF) entails complex pathophysiological processes and complicated mechanisms. It is a type of lung disease that has no known cure. The disease's chronic inflammatory response is triggered by the abnormal activation of alveolar cells that create mediators that promote the development of myofibroblast and fibroblast foci. Usually, there is an excessive level of collagens and extracellular matrix deposition that lead to the destruction of the lung's architecture. The cause and pathogenesis of IPF are relatively complicated and unknown. The role of inflammation in the pathogenesis of IPF is still controversial. If only inflammation was the only crucial element to the disease events, lung fibrosis pathology would mean an influx of inflammatory cells, and the disease would act in response to immunosuppression. However, neither of these is true. Recent studies indicate that the pathophysiology of the disease is more a consequence of fibroblast dysfunction than poorly modulated inflammation. A broad range of factors has been recognized as crucial mediators in fibrosis. This article does not intend to deliver a comprehensive review of the molecular mechanisms in IPF but will concentrate on specific topics relating to IPF pathogenesis with relevance to immune modulation. In addition, we focus on the key mediators driving the pathogenesis of pulmonary fibrosis irrespective of their etiology, in conjunction with an overview of how these studies can be translated into appropriate or future diagnostic/therapeutic applications.

Parkinson's disease (PD) is a progressive condition that affects both the central nervous system and other body parts that are controlled by the nervous system. PD is characterized by brain dopaminergic neurons loss and, at present, there are only symptomatic treatments available to alleviate the effects of the disease. With extensive research, new insights have led to defining PD as a multi-system disorder with immune dysfunction playing a dominant part in the disease pathogenesis as well as its progression. Neuroinflammation in PD leads to neurodegeneration, which is, in turn, regulated by the peripheral adaptive immunity, with CD4+ T cells being a significant player. Patients with PD have diverse CD4+ T cell phenotypes and functional profiles. These phenotypes vary, from being proinflammatory (Th1 and Th17) to anti-inflammatory (Th2 and Tregs). This report focuses on reviewing the expression of CD4+ T cells in PD and its role in the prognosis and treatment of PD.

Chalcones are the basic chemical structural predecessors of flavonoids and isoflavonoids, frequently available in many innately arising compounds. Chalcones and their counter parts have drawn the attention of many researchers because of their extensive pharmacological activities with therapeutic potential against various clinical conditions, especially for anticancer activity. The chalcone derivatives potentially suppress the growth of tumors through multiple mechanisms, encompassing interfering cell division, control of cell degradation, triggering cell suicide, and regulating the immune response towards cancer cells and inflammatory mediators. The benefits of chalcones are consistent that researchers develop chalcone derivatives asnovel cancer therapeutic agents. Combination therapy (chalcone derivatives with other chemotherapeutic agents) is even more effective in curing colon cancer. The preclinical findings of treating cancer cells with chalone derivatives were encouraging suggesting their potential use clinically in cancer patients. However, further investigations and a complete study of the degree of toxicity associated with chalcone derivatives are required. The current review summarizes the pharmacological and immunological properties of chalcones and their anticancer activities with their possible mechanisms of action in colon cancer.

Follicular regulatory T (TFR) cells are a population of CD4+ T-cells that concomitantly express markers for regulatory T-cells and follicular helper T (TFH) cells, and have been predominantly implicated in the regulation of humoral immunity via their suppressive functions. Rapid and robust progress has been made in the field of TFR cell research since the discovery of this subset over a decade ago. However, there is still a significant gap in our understanding of the mechanisms underlying the phenotypic and functional heterogeneity of TFR cells under various physiologic and pathologic settings. In this review article, we aim to highlight the most up-to-date concepts and investigations in both experimental animal models and human studies to provide a perspective on our understanding of TFR biology with particular emphasis on these cells in the context of disease settings.

Regulatory T cells (Tregs), a fraction of CD4+ T cells with immunosuppressive characteristics, are strongly linked to a number of inflammatory and autoimmune disorders. Furthermore, it also contributes to the development of tumors. Tregs infiltrate into the tumor microenvironment (TME), dampen the anti-tumor immune reaction, and facilitate tumoral immune escape. Besides the well-known hemostatic roles, mounting evidence indicates that platelets may also function as immune cells and engage in cancer immune escape. In addition, substantial evidence shows that platelets or platelet-derived mediators can regulate the proliferation, differentiation, and functions of many immune cells. Platelets also play important roles in promoting tumor cell proliferation and helping tumor cells evade immune surveillance. Here we summarize the regulatory effects of platelets in Treg proliferation, differentiation and functions and highlight the potential synergistic roles of platelets and Tregs in tumor cell immune escape.