The chemokine receptor CCR5 genetic polymorphism and expression in rheumatoid arthritis patients

Kohem, Charles Lubianca; Brenol, João Carlos Tavares; Xavier, Ricardo Machado; Bredemeier, Markus; Brenol, Claiton Viegas; Silva, T. L. Dedavid e; Mello, Adriana; Cañedo, Andrés Delgado; Neves, Andrei Gibbon; Chies, José Artur Bogo

doi:10.1080/03009740701393999

Cited by 26 publications

(30 citation statements)

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“…However, the role of this mutation status in autoimmune diseases evaluated in different populations was conflicting. While some studies showed a protective effect of the CCR5Δ32 variant on rheumatoid arthritis susceptibility [13,14]; others demonstrated lack of association of this deletion with rheumatoid arthritis [15], SLE, lupus nephritis, and disease severity [16,17]. In juvenile idiopathic arthritis subtypes, the CCR5Δ32 does not have a protective effect, but instead it could be a factor associated with more inflammatory forms of the disease [18].…”

Section: Introductionmentioning

confidence: 99%

CCR5Δ32 (rs333) polymorphism is associated with the susceptibility to systemic lupus erythematosus in female Brazilian patients

et al. 2015

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The role of CCR5Δ32 (rs333) polymorphism in the pathogenesis of systemic lupus erythematosus (SLE) has been evaluated worldwide. The aim of this study was to determine the association between CCR5Δ32 polymorphism with the susceptibility to SLE and the activity of disease in female Southern Brazilian patients. The study enrolled 169 female SLE patients and 132 unrelated female healthy individuals. Baseline clinical, laboratorial characteristics, and the SLE activity (determined using the SLEDAI) were evaluated according to the CCR5Δ32 genotypes. The CCR5Δ32 polymorphism was determined from genomic DNA using a polymerase chain reaction. The frequencies of the genotypes CCR5/CCR5, CCR5/CCR5Δ32, and CCR5Δ32/CCR5Δ32 were 87.6, 11.8, and 0.6 %, respectively, among the patients and 96.2, 3.8, and 0.0 %, respectively, among the controls [CCR5/CCR5 vs. CCR5/CCR5Δ32 + CCR5Δ32/CCR5Δ32: p = 0.0081, odds ratio 3.604 (95 % confidence interval 1.321-9.4836)]. The frequencies of the CCR5 and the CCR5Δ32 alleles were 93.2 and 6.8 % among the patients, and 98.1 and 1.9 % among the controls, respectively (p = 0.0047, OR 3.758, 95 % CI 1.409-10.80). Patients carrying the genotypes with the CCR5Δ32 allele presented earlier age of onset of disease (p = 0.0293) and higher levels of anti-dsDNA (p = 0.0255) than those carrying the wild-type genotype. When the analysis was adjusted for ethnicity, only the age at onset of disease remained significant (p > 0.05). The results suggest that the CCR5Δ32 polymorphism might be associated with SLE genetic predisposition among female Brazilian patients and the age at onset of the disease; however, this genetic variant was not associated with the activity of SLE in this population.

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Section: Introductionmentioning

confidence: 99%

CCR5Δ32 (rs333) polymorphism is associated with the susceptibility to systemic lupus erythematosus in female Brazilian patients

et al. 2015

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“…In rheumatoid arthritis, CCR5 + monocytes are found in the synovial fluid (Kohem et al, 2007) as the receptor plays a role in the inflammatory process. A meta-analysis showed that the Δ32 mutation provides protection in the latter disease (Prahalad, 2006), as the severity of the disease is reduced (Scheibel et al, 2008).…”

Section: Role Of Ccr5 Deficiency In Diseasementioning

confidence: 99%

C-C chemokine receptor type five (CCR5): An emerging target for the control of HIV infection

Barmania

Pepper

2013

Applied & Translational Genomics

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When HIV was initially discovered as the causative agent of AIDS, many expected to find a vaccine within a few years. This has however proven to be elusive; it has been approximately 30 years since HIV was first discovered, and a suitable vaccine is still not in effect. In 2009, a paper published by Hutter et al. reported on a bone marrow transplant performed on an HIV positive individual using stem cells that were derived from a donor who was homozygous for a mutation in the CCR5 gene known as CCR5 delta-32 (Δ32) (Hütter et al., 2009). The HIV positive individual became HIV negative and remained free of viral detection after transplantation despite having halted anti-retroviral (ARV) treatment. This review will focus on CCR5 as a key component in HIV immunity and will discuss the role of CCR5 in the control of HIV infection.

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“…In RA an increased expression of Fc receptors and an increased adhesion to the extracellular matrix has been described [29,30]. In addition, an activated population of CCR5+ monocytes was found in the synovial fluid of RA patients indicative for a role of these cells in the pathogenesis of RA [31,32]. The relationship between disease activity and an enhanced expression of the Dipeptidyl Peptidase IV density on monocytes of RA patients also underscores the contribution of abnormally functioning monocytes to the disease development [33].…”

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confidence: 95%

Monocyte Gene Expression Signatures in Rheumatic Diseases: Biomarkers for Disease Activity and Tools for Diagnosis and Classification

Brkić¹,

Olthof²,

Drexhage³

et al. 2010

TOARTHJ

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Monocytes migrate through the blood to the peripheral tissues, where they can develop into dendritic cells (DC) and macrophages. Studies on the phenotype of peripheral blood monocytes in rheumatic diseases revealed changes in the number of CD16+ monocytes and in the adhesive, chemotactic, antigen presenting and inflammatory properties of the cells. However, these studies often resulted in fragmented and inconsistent data and are hampered by the heterogeneity and overlap of the rheumatic diseases.By microarray analysis, changes in gene expression-profiles are detectable and subsequent correlation of the data reveals functional pathways forming a "gene expression signature". Determination of monocyte gene expression signatures in patient groups with rheumatic diseases has resulted in the detection of an Interferon (IFN) Type I induced signature in subgroups of patients with rheumatoid arthritis, Sjögren's Syndrome, systemic sclerosis and systemic lupus erythematosus. We assume that such profiling, which is robust, will lead to the development of better classification criteria and an insight into at least one functional pathogenic pathway leading to disease, i.e. the one mediated by IFN type 1.Keywords: Monocytes, IFN type I, Rheumatic diseases, Sjogren's Syndrome. MONOCYTES AND THE MONONUCLEAR PHAGO-CYTE SYSTEM (MPS)Monocytes are part of the Mononuclear Phagocyte System (MPS) system. Cells of the MPS system are thought to originate from pro-monocytes in the bone marrow and to migrate as monocytes through the blood to the peripheral tissues, where they replenish the pool of tissue and inflammatory macrophages. In addition, monocytes can function as precursors of the so-called monocyte-derived dendritic cells (DC). DC and macrophages are present in virtually all tissues and play an important role in tissue homeostasis (growth and function of parenchymal cells), the removal of debris and the regulation of the immune response. In addition to the blood monocyte as a precursor for tissue macrophages and DC, evidence is accumulating that in many tissues monocyte-like precursors for macrophages and DC are present locally. Under steady state conditions, DC and tissue macrophages are in a tolerogenic state, interacting with T cells in such a way that the induction of autoimmune responses is prevented by a preferential generation of tolerogenic regulator T cells. Under inflammatory conditions DC and macrophages can initiate effector T cells responses resulting in the induction of specific immunity and the ultimate elimination of pathogens. Monocytes can be divided into different subsets according to phenotype and function [1]. In humans, two populations have been distinguished based upon the expression of CD14 and CD16. The majority of monocytes is CD14+ and CD16-, while approximately 10% of the monocytes is CD14+ and CD16+. Further phenotypic characterization of the monocyte subsets revealed that the *Address correspondence to this author at the Department of Immunology, Erasmus MC, Rotterdam, The Netherlands; Tel...

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The chemokine receptor CCR5 genetic polymorphism and expression in rheumatoid arthritis patients

Cited by 26 publications

References 32 publications

CCR5Δ32 (rs333) polymorphism is associated with the susceptibility to systemic lupus erythematosus in female Brazilian patients

CCR5Δ32 (rs333) polymorphism is associated with the susceptibility to systemic lupus erythematosus in female Brazilian patients

C-C chemokine receptor type five (CCR5): An emerging target for the control of HIV infection

Monocyte Gene Expression Signatures in Rheumatic Diseases: Biomarkers for Disease Activity and Tools for Diagnosis and Classification

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