scholarly journals Chemokines

2007 ◽  
Vol 7 ◽  
pp. 224-232 ◽  
Author(s):  
Richard Horuk
Keyword(s):  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Chemokine Receptors ◽  
Short Review ◽  
Host Defence ◽  
Therapeutic Approaches ◽  
A Site ◽  
Hiv 1

Chemokines are a family of polypeptides that direct the migration of leukocytestoward a site of infection. They play a major role in autoimmune disease and chemokine receptors have recently been found to mediate HIV-1 fusion. In this short review we examine the role of chemokines in host defence and in the pathophysiology of autoimmune diseases. We conclude by discussing various therapeutic approaches that target chemokine receptors and that could be beneficial in disease.

scholarly journals Chemokines: understanding their role in T-lymphocyte biology

1998 ◽  
Vol 333 (3) ◽  
pp. 457-470 ◽  
Author(s):  
Stephen G. WARD ◽  
John WESTWICK
Keyword(s):  
T Lymphocytes ◽  
Chemokine Receptors ◽  
Protein Tyrosine Kinase ◽  
Cell Function ◽  
Signalling Pathways ◽  
Cc Chemokine ◽  
Intracellular Signalling Pathways ◽  
And Function ◽  
Hiv 1

The chemokines are a complex superfamily of small, secreted proteins that were initially characterized through their chemotactic effects on a variety of leucocytes. The superfamily is divided into families based on structural and genetic considerations and have been termed the CXC, CC, C and CX3C families. Chemokines from these families have a key role in the recruitment and function of T lymphocytes. Moreover, T lymphocytes have also been identified as a source of a number of chemokines. T lymphocytes also express most of the known CXC and CC chemokine receptors to an extent that depends on their state of activation/differentiation and/or the activating stimuli. The expression of two chemokine receptors, namely CXCR4 and CCR5, together with the regulated production of their respective ligands, appears to be extremely important in determining sensitivity of T cells to HIV-1 infection. The intracellular events which mediate the effects of chemokines, particularly those elicited by the CC chemokine RANTES, include activation of both G-protein- and protein tyrosine kinase-coupled signalling pathways. The present review describes our current understanding of the structure and expression of chemokines and their receptors, the effects of chemokines on T-cell function(s), the intracellular signalling pathways activated by chemokines and the role of certain chemokines and chemokine receptors in determining sensitivity to HIV-1 infection.

scholarly journals Role of Th22 Cells in the Pathogenesis of Autoimmune Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Qi Jiang ◽  
Guocan Yang ◽  
Fan Xiao ◽  
Jue Xie ◽  
Shengjun Wang ◽  
...  
Keyword(s):  
Autoimmune Diseases ◽  
Chemokine Receptors ◽  
Inflammatory Diseases ◽  
Biological Effects ◽  
Cell Subset ◽  
Interferon Γ ◽  
Th22 Cells ◽  
Tnf Α ◽  
Ifn Γ

Upon antigenic stimulation, naïve CD4+T cells differentiate into different subsets and secrete various cytokines to exert biological effects. Th22 cells, a newly identified CD4+T cell subset,are distinct from the Th1, Th2 and Th17 subsets. Th22 cells secrete certain cytokines such as IL-22, IL-13 and TNF-α, but not others, such as IL-17, IL-4, or interferon-γ (IFN-γ), and they express chemokine receptors CCR4, CCR6 and CCR10. Th22 cells were initially found to play a role in skin inflammatory diseases, but recent studies have demonstrated their involvement in the development of various autoimmune diseases. Here, we review research advances in the origin, characteristics and effector mechanisms of Th22 cells, with an emphasis on the role of Th22 cells and their main effector cytokine IL-22 in the pathogenesis of autoimmune diseases. The findings presented here may facilitate the development of new therapeutic strategies for targeting these diseases.

scholarly journals Chemokines and Chemokine Receptors in Multiple Sclerosis

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Wenjing Cheng ◽  
Guangjie Chen
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
T Cells ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Autoimmune Disease ◽  
Chemokine Receptors ◽  
Cell Subset ◽  
Small Peptide

Multiple sclerosis is an autoimmune disease with classical traits of demyelination, axonal damage, and neurodegeneration. The migration of autoimmune T cells and macrophages from blood to central nervous system as well as the destruction of blood brain barrier are thought to be the major processes in the development of this disease. Chemokines, which are small peptide mediators, can attract pathogenic cells to the sites of inflammation. Each helper T cell subset expresses different chemokine receptors so as to exert their different functions in the pathogenesis of MS. Recently published results have shown that the levels of some chemokines and chemokine receptors are increased in blood and cerebrospinal fluid of MS patients. This review describes the advanced researches on the role of chemokines and chemokine receptors in the development of MS and discusses the potential therapy of this disease targeting the chemokine network.

scholarly journals THE ASSOCIATION OF CELIAC DISEASE WITH OTHER AUTOIMMUNE DISEASES IN CHILDREN

2017 ◽  
pp. 023
Author(s):  
Jelisaveta Maksimović ◽  
Zlatko Djurić
Keyword(s):  
Celiac Disease ◽  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Clinical Signs ◽  
Protective Role ◽  
North American Population ◽  
Gluten Free ◽  
American Population ◽  
Gastrointestinal Manifestations

Celiac disease (CD) is an autoimmune disease with estimated prevalence of 1% in European and North American population. All four components of CD autoimmunity are well known, such as: genetics, autoantigen, autoantibodies and the environmental triggers. Besides gastrointestinal manifestations, celiac disease has a wide array of extraintestinal symptoms and clinical signs. This article briefly summarizes celiac disease pathophysiology and association of celiac disease with other autoimmune diseases in children. It puts emphasis on possible protective role of gluten-free diet for the development of other autoimmune diseases in patients with celiac disease.

scholarly journals Evidence for a potential role of miR-1908-5p and miR-3614-5p in autoimmune disease risk using genome-wide analyses

2018 ◽  
Author(s):  
Inken Wohlers ◽  
Lars Bertram ◽  
Christina M. Lill
Keyword(s):  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Disease Risk ◽  
Association Studies ◽  
Microrna Expression ◽  
Next Generation Sequencing Data ◽  
Genome Wide Association Studies ◽  
Functional Variants ◽  
Genome Wide

AbstractGenome-wide association studies (GWAS) have identified a large number of genetic risk loci for autoimmune diseases. However, the functional variants underlying these disease associations remain largely unknown. There is evidence that microRNA-mediated regulation may play an important role in this context. Therefore, we assessed whether autoimmune disease loci unfold their effects via altering microRNA expression in relevant immune cells.To this end, we performed microRNA expression quantitative trait loci (eQTL) analyses across 115 GWAS regions associated with 12 autoimmune diseases using next-generation sequencing data of 345 lymphoblastoid cell lines. Statistical analyses included the application and extension of a recently proposed framework (joint likelihood mapping), to microRNA expression data and microRNA target gene enrichment analyses of relevant GWAS data.Overall, only a minority of autoimmune disease risk loci may exert their pathophysiologic effects by altering miRNA expression based on JLIM. However, detailed functional fine-mapping revealed two independent GWAS regions harboring autoimmune disease risk SNPs with significant effects on microRNA expression. These relate to SNPs associated with Crohn’s disease (CD; rs102275) and rheumatoid arthritis (RA; rs968567), which affect the expression of miR-1908-5p (prs102275=1.44e-20, prs968567=2.54e-14). In addition, an independent CD risk SNP, rs3853824, was found to alter the expression of miR-3614-5p (p=5.70e-7). To support these findings, we demonstrate that GWAS signals for RA and CD were enriched in genes predicted to be targeted by both miRNAs (all with p<0.05).In summary, our study points towards a pathophysiological role of miR-1908-5p and miR- 3614-5p in autoimmunity.

Human Galectin-1 and Its Inhibitors: Privileged Target for Cancer and HIV

2019 ◽  
Vol 19 (16) ◽  
pp. 1369-1378 ◽  
Author(s):  
Narella Sridhar Goud ◽  
P.S. Lakshmi Soukya ◽  
Mahammad Ghouse ◽  
Daipule Komal ◽  
Ravi Alvala ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Viral Entry ◽  
Immune Escape ◽  
Specific Binding ◽  
Therapeutic Approaches ◽  
Therapeutic Drugs ◽  
Kinetics Of ◽  
Structural Insights ◽  
Hiv 1

Galectin 1(Gal-1), a β-galactoside binding mammalian lectin of 14KDa, is implicated in many signalling pathways, immune responses associated with cancer progression and immune disorders. Inhibition of human Gal-1 has been regarded as one of the potential therapeutic approaches for the treatment of cancer, as it plays a major role in tumour development and metastasis by modulating various biological functions viz. apoptosis, angiogenesis, migration, cell immune escape. Gal-1 is considered as a biomarker in diagnosis, prognosis and treatment condition. The overexpression of Gal-1 is well established and seen in many types of cancer progression like osteosarcoma, breast, lung, prostate, melanoma, etc. Gal-1 greatly accelerates the binding kinetics of HIV-1 to susceptible cells, leading to faster viral entry and a more robust viral replication by specific binding of CD4 cells. Hence, the Gal-1 is considered a promising molecular target for the development of new therapeutic drugs for cancer and HIV. The present review laid emphasis on structural insights and functional role of Gal-1 in the disease, current Gal-1 inhibitors and future prospects in the design of specific Gal-1 inhibitors.

Role Of Chemokine Receptors In Hiv-1 Infection And Pathogenesis

1999 ◽  
pp. 233-267 ◽  
Author(s):  
Ted M. Ross ◽  
Paul D. Bieniasz ◽  
Bryan R. Cullen
Keyword(s):  
Chemokine Receptors ◽  
Hiv 1

scholarly journals Therapeutic Application of Exosomes in Inflammatory Diseases

2021 ◽  
Vol 22 (3) ◽  
pp. 1144
Author(s):  
Ju Hun Suh ◽  
Hyeon Su Joo ◽  
Eun Be Hong ◽  
Hyeon Ji Lee ◽  
Jung Min Lee
Keyword(s):  
Immune System ◽  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Human Body ◽  
Therapeutic Strategy ◽  
State Of The Art ◽  
Inflammatory Diseases ◽  
Defense System ◽  
Therapeutic Application

Immunomodulation is on the cusp of being an important therapy for treating many diseases, due to the significant role of the immune system in defending the human body. Although the immune system is an essential defense system, overactivity can result in diverse sicknesses such as inflammation and autoimmune disease. Exosomes are emerging as a state-of-the-art therapeutic strategy for treating an overactive immune system. Thus, in this review, we will thoroughly review therapeutic applications of exosomes in various inflammatory and autoimmune diseases. Finally, issues for an outlook to the future of exosomal therapy will be introduced.

Intracrinology and gastric cancer

2017 ◽  
Vol 86 (1) ◽  
pp. 76
Author(s):  
Bartosz Adam Frycz ◽  
Paweł Piotr Jagodziński
Keyword(s):  
Gastric Cancer ◽  
Steroid Hormones ◽  
Malignant Tumors ◽  
Current Knowledge ◽  
Short Review ◽  
Therapeutic Approaches ◽  
Peripheral Tissues ◽  
Expression Of Genes ◽  
Genes Encoding

Overall incidence of gastric cancer (GC) in most populations is approximately two times higher in men than women. Therefore, steroid hormones are suspect to play a role in gastric carcinogenesis. Large amounts of steroid hormones in postmenopausal women and older men are synthesized in peripheral tissues through enzymatic conversion of blood derived precursors into active estrogens and androgens in so called, intracrine mechanism. Moreover, abnormal expression of genes encoding steroidogenic enzymes was shown in numerous malignant tumors including GC. These abnormalities can be associated with deregulated production of steroid hormones in gastric tissue and thus affect the risk of GC. For that reason this short review aims to summarize the current knowledge about the expression of genes involved in metabolism of steroid hormones in normal and malignant gastric mucosa and thus, estimate the potential of these tissues to intracrine synthesis of steroid hormones. This findings could be useful in understanding the role of above mechanism in GC and could help to find therapeutic approaches in future.

TREX1 As a Potential Therapeutic Target for Autoimmune and Inflammatory Diseases

2019 ◽  
Vol 25 (30) ◽  
pp. 3239-3247 ◽  
Author(s):  
Sha-Sha Tao ◽  
Guo-Cui Wu ◽  
Qin Zhang ◽  
Tian-Ping Zhang ◽  
Rui-Xue Leng ◽  
...  
Keyword(s):  
Autoimmune Disease ◽  
Autoimmune Diseases ◽  
Therapeutic Target ◽  
Mammalian Cells ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Autoimmune Response ◽  
Autoimmune And Inflammatory Diseases ◽  
Functional Mechanisms

Background and Objectives: The 3’ repair exonuclease 1 (TREX1) gene is the major DNA-specific 3’–5 ’exonuclease of mammalian cells which reduces single- and double-stranded DNA (ssDNA and dsDNA) to prevent undue immune activation mediated by the nucleic acid. TREX1 is also a crucial suppressor of selfrecognition that protects the host from inappropriate autoimmune activations. It has been revealed that TREX1 function is necessary to prevent host DNA accumulating after cell death which could actuate an autoimmune response. In the manuscript, we will discuss in detail the latest advancement to study the role of TREX1 in autoimmune disease. Methods: As a pivotal cytoprotective, antioxidant, anti-apoptotic, immunosuppressive, as well as an antiinflammatory molecule, the functional mechanisms of TREX1 were multifactorial. In this review, we will briefly summarize the latest advancement in studying the role of TREX1 in autoimmune disease, and discuss its potential as a therapeutic target for these diseases. Results: Deficiency of TREX1 in human patients and murine models is characterized by systemic inflammation and the disorder of TREX1 functions drives inflammatory responses leading to autoimmune disease. Moreover, much more studies revealed that mutations in TREX1 have been associated with a range of autoimmune disorders. But it is also unclear whether the mutations of TREX1 play a causal role in the disease progression, and whether manipulation of TREX1 has a beneficial effect in the treatment of autoimmune diseases. Conclusion: Integration of functional TREX1 biology into autoimmune diseases may further deepen our understanding of the development and pathogenesis of autoimmune diseases and provide new clues and evidence for the treatment of autoimmune diseases.

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