Mutation-Induced Functional Alterations of CCR6

Julian, Bina; Gao, Kevin MingJie; Harwood, Benjamin N.; Beinborn, Martin; Kopin, Alan S.

doi:10.1124/jpet.116.237669

Cited by 12 publications

(11 citation statements)

References 54 publications

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“…Genetics of autoimmune diseasesContributes to the incomplete clearance of immune complexes 60 PTPN221p 13.3-13.1 Increases the formation and deposition of immune complexes SNP) array genotyping, numerous candidate genes have been identified,67 but few have been studied for their biological function. The most relevant non-HLA genes associated with RA include PTPN22, 68 IL23R, 69 TRAF1, 70 CTLA4, 71 IRF5, 72 STAT4, 73 CCR6 (ref 74). and PADI4 71,75.…”

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confidence: 99%

Genetic and epigenetic influences on the loss of tolerance in autoimmunity

Zhang

2018

Cell Mol Immunol

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Immunological tolerance loss is fundamental to the development of autoimmunity; however, the underlying mechanisms remain elusive. Immune tolerance consists of central and peripheral tolerance. Central tolerance, which occurs in the thymus for T cells and bone marrow for B cells, is the primary way that the immune system discriminates self from non-self. Peripheral tolerance, which occurs in tissues and lymph nodes after lymphocyte maturation, controls self-reactive immune cells and prevents over-reactive immune responses to various environment factors. Loss of tolerance results in autoimmune disorders, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), type 1 diabetes (T1D) and primary biliary cirrhosis (PBC). The etiology and pathogenesis of autoimmune diseases are highly complicated. Both genetic predisposition and epigenetic modifications are implicated in the loss of tolerance and autoimmunity. In this review, we will discuss the genetic and epigenetic influences on tolerance breakdown in autoimmunity. Genetic and epigenetic influences on autoimmune diseases, such as SLE, RA, T1D and PBC, will also be briefly discussed.

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confidence: 99%

Genetic and epigenetic influences on the loss of tolerance in autoimmunity

Zhang

2018

Cell Mol Immunol

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“…8 In the urban population, CCR6 mRNA expression was increased after the cleaning procedures, which is in agreement with findings showing that this mediator is essential for the recruitment of both proinflammatory IL-17-producing helper T cells (Th17) and Treg cells to sites of inflammation. 35 The null hypothesis was accepted; minor regulatory variants that have arisen over time in response to environmental factors caused significant quantitative genetic variability among hosts in the regulation of the periapical immune response. Because the functional plasticity and redundancy of the immune system complicate the experimental study of each of its components, the results of this study contribute to the overall understanding of the specific immune responses that predominate in the periapical area in each individualized urban and indigenous population after instituting clinical endodontic therapy.…”

Section: Discussionmentioning

confidence: 99%

Influence of genetic regulatory effects modified by environmental immune activation on periapical disease

et al. 2019

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The objective of this study was to compare the periradicular responses in endodontic infections among members of two populations: an urban Brazilian population and a non-mixed indigenous population. Samples were collected immediately and 7 days after the cleaning and shaping procedures (after reducing the intracanal microbial load) in an attempt to characterize the expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-9, interferon (IFN)-γ, IL-17, IL-10, and the chemokines CXCR4, CCL2/monocyte chemotactic protein (MCP)-1, and CCR6. The endogenous cytokine and chemokine expression levels were analyzed using real-time PCR. Only the urban population showed a significant increase in TNF-α, CCL2/MCP-1, CXCR4, and CCR6 expression following the cleaning and shaping of the root canal system. The IFN-γ levels were increased at the 2 nd collection (p < 0.05) in the indigenous population. In turn, a significant increase in IL-10 and IL-17 expression (p < 0.05) was observed after the cleaning and shaping procedures (2 nd collection) in both populations. No significant differences in the IL-1β, IL-9, and CCL4 expression levels were observed between the 1 st and 2 nd collections in both populations. The results demonstrate a cytokine and chemokine expression profile that is specific to each analyzed population. However, immune modulation mediated by IL-10 began on the 7 th day after the beginning of the endodontic treatment in both populations.

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“…A possible role in pathogenesis is thus highlighted in CCR6 in promoting inflammation at the joints [ 41 , 42 , 43 ]. Ccr6 single nucleotide polymorphisms (SNPs) have demonstrated diminished basal and ligand induced Gαi protein signaling which predisposes individuals to diseases such as rheumatoid arthritis [ 44 ].…”

Section: Ccr6 and Ccl20 In Health And Diseasementioning

confidence: 99%

Pleiotropic Immune Functions of Chemokine Receptor 6 in Health and Disease

Ranasinghe

Eri

2018

Medicines

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C-C chemoattractant cytokine (chemokine) receptor 6 (CCR6) and its exclusive binding molecule CCL20 is an extremely important chemokine receptor-ligand pair which controls cell migration and immune induction during inflammatory disease. Not many scientific studies have been undertaken to study its immune mechanisms in detail, but its unique contribution to steady state cell chemotaxis in upholding immune tolerance and regulating immune homeostasis during inflammation is evident in multiple systems in the human body, including skin, liver, lung, kidney, brain, eye, joints, gonads and the gut. The role of CCR6 is constitutively expressed as a series of much debilitating severe inflammatory and autoimmune diseases, Human Immunodeficiency Virus (HIV) and cancer metastasis. CD4+ T cells, the central organizers of adaptive immunity, are stringently mobilized by the CCR6/CCL20 axis also induced by cytokines and a host of other factors in a carefully executed immune modulation scenario, to bring about a delicate balance between inflammation inducing TH17 cells and regulatory Treg cells. Although the exact immune regulatory role is not elucidated as yet, the CCR6/CCL20 axis is implicated as a front runner which determines the polarization of TH17 and regulatory Treg cells, upon which depends the resolution or progression of many debilitating disorders. This review therefore aims at emphasizing the pleiotropic significance of the chemokines CCR6 and CCL20 in immunologic function in multiple organ systems, thereby hoping to accentuate its value in future therapeutic modalities.

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Mutation-Induced Functional Alterations of CCR6

Cited by 12 publications

References 54 publications

Genetic and epigenetic influences on the loss of tolerance in autoimmunity

Genetic and epigenetic influences on the loss of tolerance in autoimmunity

Influence of genetic regulatory effects modified by environmental immune activation on periapical disease

Pleiotropic Immune Functions of Chemokine Receptor 6 in Health and Disease

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