The -2518A>G promoter polymorphism in the CCL2 gene is not associated with systemic sclerosis susceptibility or phenotype: Results from a multicenter study of European Caucasian patients

Timothy R.D.J. Radstake; Madelon C. Vonk; Marieke Dekkers; Mascha M.V.A.P. Schijvenaars; William L. Treppichio; Robert Lafyatis; Gabriela Riemekasten; Frank van den Hoogen; Marieke J.H. Coenen

doi:10.1016/j.humimm.2008.10.012

The -2518A>G promoter polymorphism in the CCL2 gene is not associated with systemic sclerosis susceptibility or phenotype: Results from a multicenter study of European Caucasian patients

Timothy R.D.J. Radstake^*, Madelon C. Vonk, Marieke Dekkers, Mascha M.V.A.P. Schijvenaars, William L. Treppichio, Robert Lafyatis, Gabriela Riemekasten, Frank van den Hoogen, Marieke J.H. Coenen

^*Corresponding author for this work

Clinic of Rheumatology

Radboud University Nijmegen

10 Citations (Scopus)

Abstract

A single nucleotide polymorphism (SNP) of the gene encoding monocyte chemoattractant protein-1 (MCP-1, CCL2) has previously been suggested to be involved in the susceptibility of systemic sclerosis (SSc). Here we have tested whether the -2518A>G CCL2 variant is associated with SSc susceptibility and/or phenotype using a cohort of SSc patients (n = 345). Clinical data from SSc patients attending rheumatology clinics in the Netherlands and Germany was collected DNA was obtained after informed consent. The control group used (n = 272) was randomly recruited from comparable geographic regions. The -2518A>G SNP in CCL2 (rs1024611) was determined using a Taqman SNP Genotyping assay. The genotype distribution was found to be similarly distributed among SSc patients and healthy controls. In addition, no association could be detected between the genotype and the presence of antinuclear antibodies, anticentromere antibodies, and antitopoisomerase antibodies or pulmonary involvement. Our results demonstrate that the functional variant -2518A>G of CCL2 is not implicated in the susceptibility or phenotype of SSc.

Original language	English
Journal	Human Immunology
Volume	70
Issue number	2
Pages (from-to)	130-133
Number of pages	4
ISSN	0198-8859
DOIs	https://doi.org/10.1016/j.humimm.2008.10.012
Publication status	Published - 02.2009

Funding

We are greatly thankful to all of the rheumatologists and research nurses who were involved in the collection of blood. We also thank Christel Brouwer and Jasper Broen for their invaluable work regarding the isolation, measurement, and storage of DNA samples. This study was funded by Millenium Inc, a personal grant from the Netherlands Organization for Scientific Research (NWO, VENI grant T.R.), and the Young Investigators grant from EULAR (T.R.). This publication reflects solely the authors' views and not those of the supporting organizations.

Research Areas and Centers

Academic Focus: Center for Infection and Inflammation Research (ZIEL)

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.humimm.2008.10.012

Cite this

Radstake, T. R. D. J., Vonk, M. C., Dekkers, M., Schijvenaars, M. M. V. A. P., Treppichio, W. L., Lafyatis, R., Riemekasten, G., van den Hoogen, F., & Coenen, M. J. H. (2009). The -2518A>G promoter polymorphism in the CCL2 gene is not associated with systemic sclerosis susceptibility or phenotype: Results from a multicenter study of European Caucasian patients. Human Immunology, 70(2), 130-133. https://doi.org/10.1016/j.humimm.2008.10.012

@article{afb15bcaddf84b9bae4adff2e9531fcc,

title = "The -2518A>G promoter polymorphism in the CCL2 gene is not associated with systemic sclerosis susceptibility or phenotype: Results from a multicenter study of European Caucasian patients",

abstract = "A single nucleotide polymorphism (SNP) of the gene encoding monocyte chemoattractant protein-1 (MCP-1, CCL2) has previously been suggested to be involved in the susceptibility of systemic sclerosis (SSc). Here we have tested whether the -2518A>G CCL2 variant is associated with SSc susceptibility and/or phenotype using a cohort of SSc patients (n = 345). Clinical data from SSc patients attending rheumatology clinics in the Netherlands and Germany was collected DNA was obtained after informed consent. The control group used (n = 272) was randomly recruited from comparable geographic regions. The -2518A>G SNP in CCL2 (rs1024611) was determined using a Taqman SNP Genotyping assay. The genotype distribution was found to be similarly distributed among SSc patients and healthy controls. In addition, no association could be detected between the genotype and the presence of antinuclear antibodies, anticentromere antibodies, and antitopoisomerase antibodies or pulmonary involvement. Our results demonstrate that the functional variant -2518A>G of CCL2 is not implicated in the susceptibility or phenotype of SSc.",

author = "Radstake, \{Timothy R.D.J.\} and Vonk, \{Madelon C.\} and Marieke Dekkers and Schijvenaars, \{Mascha M.V.A.P.\} and Treppichio, \{William L.\} and Robert Lafyatis and Gabriela Riemekasten and \{van den Hoogen\}, Frank and Coenen, \{Marieke J.H.\}",

note = "Funding Information: We are greatly thankful to all of the rheumatologists and research nurses who were involved in the collection of blood. We also thank Christel Brouwer and Jasper Broen for their invaluable work regarding the isolation, measurement, and storage of DNA samples. This study was funded by Millenium Inc, a personal grant from the Netherlands Organization for Scientific Research (NWO, VENI grant T.R.), and the Young Investigators grant from EULAR (T.R.). This publication reflects solely the authors' views and not those of the supporting organizations. Copyright: Copyright 2009 Elsevier B.V., All rights reserved.",

year = "2009",

month = feb,

doi = "10.1016/j.humimm.2008.10.012",

language = "English",

volume = "70",

pages = "130--133",

journal = "Human Immunology",

issn = "0198-8859",

publisher = "Elsevier Inc.",

number = "2",

}

Radstake, TRDJ, Vonk, MC, Dekkers, M, Schijvenaars, MMVAP, Treppichio, WL, Lafyatis, R, Riemekasten, G, van den Hoogen, F & Coenen, MJH 2009, 'The -2518A>G promoter polymorphism in the CCL2 gene is not associated with systemic sclerosis susceptibility or phenotype: Results from a multicenter study of European Caucasian patients', Human Immunology, vol. 70, no. 2, pp. 130-133. https://doi.org/10.1016/j.humimm.2008.10.012

The -2518A>G promoter polymorphism in the CCL2 gene is not associated with systemic sclerosis susceptibility or phenotype: Results from a multicenter study of European Caucasian patients. / Radstake, Timothy R.D.J.; Vonk, Madelon C.; Dekkers, Marieke et al.
In: Human Immunology, Vol. 70, No. 2, 02.2009, p. 130-133.

Research output: Journal Articles › Journal articles › Research › peer-review

TY - JOUR

T1 - The -2518A>G promoter polymorphism in the CCL2 gene is not associated with systemic sclerosis susceptibility or phenotype: Results from a multicenter study of European Caucasian patients

AU - Radstake, Timothy R.D.J.

AU - Vonk, Madelon C.

AU - Dekkers, Marieke

AU - Schijvenaars, Mascha M.V.A.P.

AU - Treppichio, William L.

AU - Lafyatis, Robert

AU - Riemekasten, Gabriela

AU - van den Hoogen, Frank

AU - Coenen, Marieke J.H.

N1 - Funding Information: We are greatly thankful to all of the rheumatologists and research nurses who were involved in the collection of blood. We also thank Christel Brouwer and Jasper Broen for their invaluable work regarding the isolation, measurement, and storage of DNA samples. This study was funded by Millenium Inc, a personal grant from the Netherlands Organization for Scientific Research (NWO, VENI grant T.R.), and the Young Investigators grant from EULAR (T.R.). This publication reflects solely the authors' views and not those of the supporting organizations. Copyright: Copyright 2009 Elsevier B.V., All rights reserved.

PY - 2009/2

Y1 - 2009/2

N2 - A single nucleotide polymorphism (SNP) of the gene encoding monocyte chemoattractant protein-1 (MCP-1, CCL2) has previously been suggested to be involved in the susceptibility of systemic sclerosis (SSc). Here we have tested whether the -2518A>G CCL2 variant is associated with SSc susceptibility and/or phenotype using a cohort of SSc patients (n = 345). Clinical data from SSc patients attending rheumatology clinics in the Netherlands and Germany was collected DNA was obtained after informed consent. The control group used (n = 272) was randomly recruited from comparable geographic regions. The -2518A>G SNP in CCL2 (rs1024611) was determined using a Taqman SNP Genotyping assay. The genotype distribution was found to be similarly distributed among SSc patients and healthy controls. In addition, no association could be detected between the genotype and the presence of antinuclear antibodies, anticentromere antibodies, and antitopoisomerase antibodies or pulmonary involvement. Our results demonstrate that the functional variant -2518A>G of CCL2 is not implicated in the susceptibility or phenotype of SSc.

AB - A single nucleotide polymorphism (SNP) of the gene encoding monocyte chemoattractant protein-1 (MCP-1, CCL2) has previously been suggested to be involved in the susceptibility of systemic sclerosis (SSc). Here we have tested whether the -2518A>G CCL2 variant is associated with SSc susceptibility and/or phenotype using a cohort of SSc patients (n = 345). Clinical data from SSc patients attending rheumatology clinics in the Netherlands and Germany was collected DNA was obtained after informed consent. The control group used (n = 272) was randomly recruited from comparable geographic regions. The -2518A>G SNP in CCL2 (rs1024611) was determined using a Taqman SNP Genotyping assay. The genotype distribution was found to be similarly distributed among SSc patients and healthy controls. In addition, no association could be detected between the genotype and the presence of antinuclear antibodies, anticentromere antibodies, and antitopoisomerase antibodies or pulmonary involvement. Our results demonstrate that the functional variant -2518A>G of CCL2 is not implicated in the susceptibility or phenotype of SSc.

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U2 - 10.1016/j.humimm.2008.10.012

DO - 10.1016/j.humimm.2008.10.012

M3 - Journal articles

C2 - 19032966

AN - SCOPUS:59649084868

SN - 0198-8859

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JF - Human Immunology

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