Updated Progress of Interleukin-17 in Gynecological Tumors
0
Citation
0
Reference
20
Related Paper
Abstract:
Interleukin (IL)-17 is a pro-inflammatory cytokines mainly produced by activated CD4+ T lymphocytes , which involved in the immune response, inflammation and autoimmune diseases , with biological functions of strong recruitment of neutrophils, promoting a variety of cytokines release inflammatory factors and cell proliferation. Present study found that interleukin-17 is significant in tumor development .This article focus on the relationships among interleukin-17 and ovarian cancer, cervical cancer, choriocarcinoma and other gynecological tumors.
Key words:
interleukin (IL)-17; T helper cell; cancerKeywords:
Interleukin 15
Abstract Human cancer is characterized by deficits in antigen-specific immunity and intratumoral CD8+ T cells. On the other hand, inflammatory macrophages and mediators of chronic inflammation are highly prevalent in patients with late-stage cancer. Intratumoral T-cell deficiency and chronic inflammation have been linked independently to a poor prognosis in patients with cancer, and therapeutic approaches to overcome either pathology separately are in clinical testing. The anti-inflammatory cytokine interleukin (IL)-10 suppresses macrophage and proinflammatory Th17 T-cell responses by inhibiting the inflammatory cytokines IL-6 and IL-12/23. Corroborating the anti-inflammatory action of IL-10, deficiency in IL-10 leads to a stimulation of inflammatory responses and inflammatory bowel disease. The anti-inflammatory role of IL-10 fostered the assumption that IL-10 undermines the immune response to cancer. However, mice and humans deficient in IL-10 signaling develop tumors spontaneously and at high rates. Overexpression of IL-10 in models of human cancer or treatment with a pegylated IL-10 (PEG-IL-10) led to tumor rejection and long-lasting tumor immunity. IL-10 stimulates cytotoxicity of CD8+ T cells and the expression of IFN-γ in CD8+ T cells. IL-10–induced tumor rejections are dependent on the expression of IFN-γ and granzymes in tumor-resident CD8+ T cells and the upregulation of MHC molecules. These findings reconcile earlier clinical data, which showed that recombinant IL-10 increased IFN-γ and granzymes in the blood of treated individuals. PEG-IL-10 is therefore a unique therapeutic agent, which simultaneously stimulates antitumor immunity and inhibits tumor-associated inflammation. Cancer Immunol Res; 2(3); 194–9. ©2014 AACR.
Granzyme
Proinflammatory cytokine
Cancer Immunotherapy
Cite
Citations (261)
Interleukin 9
Cite
Citations (5)
Endometriosis is recognized as an inflammatory disease in which inflammatory cytokines, such as interleukin (IL)-1β and TNFα, play important roles. Immunological factors are also suggested to be involved in the pathogenesis of endometriosis. This review provides comprehensive knowledge about helper T cell (Th cell) and its specific cytokines in endometriosis. A series of our studies demonstrated the presence of Th2 cells and Th17 cells in endometriotic tissues and revealed multiple effects of IL-4 and IL-17A, cytokines secreted from respective Th cells. IL-1β induces secretion of thymic stromal lymphopoietin (TSLP), a regulator for differentiation of inflammatory Th2 cells, in endometriotic stromal cells (ESCs). IL-4 stimulates proliferation of ESCs and production of 3β-hydroxysteroid dehydrogenase Type 2, an enzyme in an estrogen production pathway, in ESCs. IL-17A stimulates IL-8 and Gro-α secretion from ESCs and proliferation of ESCs. IL-17A-induced Gro-α promotes neutrophil migration, which may contribute to the presence of neutrophils in endometriotic tissues. IL-17A also increases secretion of CCL20, a chemokine for Th17 cells, from ESCs, which seems to induce migration of Th17 cells to the endometriotic tissues and enhance the effects of IL-17A further. TNFα in combination with IL-17A synergistically enhances secretion of IL-8 and CCL-20, suggesting cooperation of inflammation and Th17 immune response. These findings suggest that IL-4 and IL-17A promote the development of endometriosis through induction of cell proliferation, inflammation, and estrogen production. It is thus also suggested that IL-4 and IL-17A would be a target of treatment of the disease.
Thymic stromal lymphopoietin
Cite
Citations (10)
Interleukin 22
Innate lymphoid cell
Cite
Citations (76)
The airway inflammation underlying asthma is regulated by a network of mutually interacting cytokines. The exact functional role of each individual cytokine in the pathogenesis of the disease remains to be fully established. Type 2 T‐helper cells are currently considered to play a crucial role in this process. In vivo animal data suggest a sequential involvement of interleukin (IL)‐4 and IL‐5 in the induction of allergen-induced airway changes. The potential role of other type 2 T‐helper cell-like cytokines in asthma is increasingly being recognized. In particular, IL‐4 and -13 display a large degree of redundancy. Whereas IL‐4 seems to be crucial in the primary allergen sensitization process, IL-13 might be more important during secondary exposure to aerosolized allergen. Animal models also indicate that T‐cell-derived cytokine production, rather than eosinophil influx or immunoglobulin‐E synthesis, is causally related to altered airway behaviour. An important aspect when evaluating the functional role of cytokines in a complex disease such as asthma is the interaction with other cytokines in the microenvironment. Increased expression of pro-inflammatory cytokines such as tumour necrosis factor‐α can further enhance the inflammatory process, and is increasingly linked to disease severity. In addition, decreased expression of immunoregulatory cytokines, including interleukin-12, interleukin-18 or interferon gamma could also strengthen the type 2 T‐helper cell-driven inflammatory process.
Cite
Citations (173)
Cite
Citations (2)
Cite
Citations (137)
The effect of systemic administration of anti-inflammatory cytokines (IL-4 and IL-10) on the development and maintenance of an anti-tumor rejection response in vivo was studied by following the growth patterns of P815.B7 tumors on B6D2F1 [(C57BI/6 x DBA/2)F1] mice. The anti-P815.B7 rejection response was found to be T cell dependent, involving both CD4 and CD8 cells. IL-4 treatment resulted in a compromised rejection response; IL-10 treatment alone had little or no effect. These results demonstrate that treatment with an anti-inflammatory cytokine can compromise an otherwise effective anti-tumor rejection response. For the anti-inflammatory cytokine IL-4, the immunosuppressive effects of the cytokine appear to outweigh any possible anti-tumor activities as have been reported using tumor cells genetically altered to produce IL-4. Relatively high systemic doses of IL-10, in contrast, were not immunosuppressive and, when given in combination with IL-4, countered the IL-4 suppressive effect. Pathologically, IL-4 treatment led to splenomegaly characterized by a marked increase in neutrophils and NK activity. The possible linkages between neutrophils, NK activity and IL-12 are discussed.
Cite
Citations (13)
Bladder cancer (BC) is the 9th most commonly diagnosed cancer worldwide, with the highest rates in developed countries. About ¾ of the patients are men. The risk of developing of malignancies increases with chronic inflammation. Chronic inflammation can be caused by infections, autoimmune diseases and other factors. In conditions of chronic inflammation, cytokines are involved in leukocyte recruitment due to enhanced expression of cell adhesion molecules and chemoattraction. Cytokines are involved in the inflammatory response, for example, they are the main determinants of cellular infiltration, cellular activation and systemic response to inflammation. It is now well established that the role of cytokines is to participate in many aspects of biology, including malignancies. Cytokines can be secreted not only by proinflammatory cells but also by stromal cells and malignant cells, thus establishing a network with various factors that may be involved in the development of BC. The progression of BC causes an imbalance between local and general immunity. The relationship between neoplastic cells and their microenvironment is essential in the proliferation and invasion of malignant cells. The purpose of this work was to determine the content of cytokines IL-1b, IL-4, IL-6, IL-10, TNF-α and IFNγ in tumor tissues, depending on the grade of cell differentiation. In our study the content of IL-1b, IL-4, IL-6, IL-10 was higher in the wall samples of bladder cancer tissues in patients with G3-4 grade BC, which may be an important characteristic of malignant cells in BC, and explain the high invasiveness of BC. The content of TNF-α, IFNγ did not significantly change depending on grade. The data of our study are consistent with the data of previous studies conducted in the study of other neoplasms, which indicate the relationship of the studied indicators with the development of cancer.
Proinflammatory cytokine
Infiltration (HVAC)
Cite
Citations (0)
Interleukin (IL)-38, a newly discovered IL-1 family cytokine, is expressed in several tissues and secreted by various cells. IL-38 has recently been reported to exert an anti-inflammatory function by binding to several receptors, including interleukin-36 receptor (IL-36R), interleukin-1 receptor accessory protein-like 1 (IL-1RAPL1), and interleukin-1 receptor 1 (IL-1R1) to block binding with other pro-inflammatory cytokines and inhibit subsequent signaling pathways; thereby regulating the differentiation and function of T cells, peripheral blood mononuclear cells, macrophages, and dendritic cells. Inflammatory autoimmune diseases, which are common immune-mediated inflammatory syndromes, are characterized by an imbalance between T helper cells (Ths), especially Th1s and Th17s, and regulatory T cells (Tregs). Recent findings have shown that abnormal expression of IL-38 in inflammatory autoimmune diseases, such as rheumatoid arthritis, psoriatic arthritis, systemic lupus erythematosus, primary Sjogren's syndrome, psoriasis, inflammatory bowel disease, hidradenitis suppurativa, ankylosing spondylitis, and glaucoma, involves Th1s, Th17s, and Tregs. In this review, the expression, regulation, and biological function of IL-38 are discussed, as are the roles of IL-38 in various inflammatory autoimmune disorders. Current data support that the IL-38/IL-36R and/or IL-38/IL-1RAPL1 axis primarily play an anti-inflammatory role in the development and resolution of inflammatory autoimmune diseases and indicate a possible therapeutic benefit of IL-38 in these diseases.
Interleukin-23
Cite
Citations (84)