Lack of association of CCR2-64I and CCR5-Δ32 with type 1 diabetes and latent autoimmune diabetes in adults

Giovanni Gambelunghe; Mehran Ghaderi; Annalisa Brozzetti; Paola Del Sindaco; Babeck Gharizadeh; Paul Nyren; Peter Hjelmström; Liene Nikitina-Zake; Carani B. Sanjeevi; Alberto Falorni

doi:10.1016/S0198-8859(03)00064-8

Lack of association of CCR2-64I and CCR5-Δ32 with type 1 diabetes and latent autoimmune diabetes in adults

Giovanni Gambelunghe, Mehran Ghaderi, Annalisa Brozzetti, Paola Del Sindaco, Babeck Gharizadeh, Paul Nyren, Peter Hjelmström, Liene Nikitina-Zake, Carani B. Sanjeevi, Alberto Falorni

Research output: Contribution to journal › Article › peer-review

14 Citations (Scopus)

Abstract

It is well known that type 1 diabetes mellitus (T1DM) is a complex genetic disease resulting from the autoimmune destruction of pancreatic beta cells. Several genes have been associated with susceptibility and/or protection for T1DM, but the disease risk is mostly influenced by genes located in the class II region of the major histocompatibility complex. The attraction of leukocytes to tissues is essential for inflammation and the beginning of autoimmune reaction. The process is controlled by chemokines, which are chemotactic cytolines. Some studies have shown that CCR2-64I and CCR5-Δ32 might be important for protection of susceptibility to some immunologically-mediated disorders. In the present study, we demonstrate the lack of association between CCR2-64I and CCR5-Δ32 gene polymorphism and TIDM and we desrcibe a new method for a simple and more precise genotyping of the CCR2 gene.

Original language	English
Pages (from-to)	629-632
Number of pages	4
Journal	Human Immunology
Volume	64
Issue number	6
DOIs	https://doi.org/10.1016/S0198-8859(03)00064-8
Publication status	Published - 1 Jun 2003
Externally published	Yes

Keywords*

CCR2-64I gene
CCR5-Δ32 gene
Chemokine
Latent autoimmune diabetes of the adult
Type 1 diabetes

Field of Science*

1.6 Biological sciences
3.1 Basic medicine
3.2 Clinical medicine

Publication Type*

1.1. Scientific article indexed in Web of Science and/or Scopus database

UN SDGs

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

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10.1016/S0198-8859(03)00064-8

Cite this

@article{ac47ac3f8a194075b689121fa7a29380,

title = "Lack of association of CCR2-64I and CCR5-Δ32 with type 1 diabetes and latent autoimmune diabetes in adults",

abstract = "It is well known that type 1 diabetes mellitus (T1DM) is a complex genetic disease resulting from the autoimmune destruction of pancreatic beta cells. Several genes have been associated with susceptibility and/or protection for T1DM, but the disease risk is mostly influenced by genes located in the class II region of the major histocompatibility complex. The attraction of leukocytes to tissues is essential for inflammation and the beginning of autoimmune reaction. The process is controlled by chemokines, which are chemotactic cytolines. Some studies have shown that CCR2-64I and CCR5-Δ32 might be important for protection of susceptibility to some immunologically-mediated disorders. In the present study, we demonstrate the lack of association between CCR2-64I and CCR5-Δ32 gene polymorphism and TIDM and we desrcibe a new method for a simple and more precise genotyping of the CCR2 gene.",

keywords = "CCR2-64I gene, CCR5-Δ32 gene, Chemokine, Latent autoimmune diabetes of the adult, Type 1 diabetes",

author = "Giovanni Gambelunghe and Mehran Ghaderi and Annalisa Brozzetti and {Del Sindaco}, Paola and Babeck Gharizadeh and Paul Nyren and Peter Hjelmstr{\"o}m and Liene Nikitina-Zake and Sanjeevi, {Carani B.} and Alberto Falorni",

note = "Funding Information: This study was supported by funds from the SVENSKA Institutet, Stockholm, Sweden, to G. Gambelunghe.",

year = "2003",

month = jun,

day = "1",

doi = "10.1016/S0198-8859(03)00064-8",

language = "English",

volume = "64",

pages = "629--632",

journal = "Human Immunology",

issn = "0198-8859",

publisher = "Elsevier Inc.",

number = "6",

}

TY - JOUR

T1 - Lack of association of CCR2-64I and CCR5-Δ32 with type 1 diabetes and latent autoimmune diabetes in adults

AU - Gambelunghe, Giovanni

AU - Ghaderi, Mehran

AU - Brozzetti, Annalisa

AU - Del Sindaco, Paola

AU - Gharizadeh, Babeck

AU - Nyren, Paul

AU - Hjelmström, Peter

AU - Nikitina-Zake, Liene

AU - Sanjeevi, Carani B.

AU - Falorni, Alberto

N1 - Funding Information: This study was supported by funds from the SVENSKA Institutet, Stockholm, Sweden, to G. Gambelunghe.

PY - 2003/6/1

Y1 - 2003/6/1

N2 - It is well known that type 1 diabetes mellitus (T1DM) is a complex genetic disease resulting from the autoimmune destruction of pancreatic beta cells. Several genes have been associated with susceptibility and/or protection for T1DM, but the disease risk is mostly influenced by genes located in the class II region of the major histocompatibility complex. The attraction of leukocytes to tissues is essential for inflammation and the beginning of autoimmune reaction. The process is controlled by chemokines, which are chemotactic cytolines. Some studies have shown that CCR2-64I and CCR5-Δ32 might be important for protection of susceptibility to some immunologically-mediated disorders. In the present study, we demonstrate the lack of association between CCR2-64I and CCR5-Δ32 gene polymorphism and TIDM and we desrcibe a new method for a simple and more precise genotyping of the CCR2 gene.

AB - It is well known that type 1 diabetes mellitus (T1DM) is a complex genetic disease resulting from the autoimmune destruction of pancreatic beta cells. Several genes have been associated with susceptibility and/or protection for T1DM, but the disease risk is mostly influenced by genes located in the class II region of the major histocompatibility complex. The attraction of leukocytes to tissues is essential for inflammation and the beginning of autoimmune reaction. The process is controlled by chemokines, which are chemotactic cytolines. Some studies have shown that CCR2-64I and CCR5-Δ32 might be important for protection of susceptibility to some immunologically-mediated disorders. In the present study, we demonstrate the lack of association between CCR2-64I and CCR5-Δ32 gene polymorphism and TIDM and we desrcibe a new method for a simple and more precise genotyping of the CCR2 gene.

KW - CCR2-64I gene

KW - CCR5-Δ32 gene

KW - Chemokine

KW - Latent autoimmune diabetes of the adult

KW - Type 1 diabetes

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U2 - 10.1016/S0198-8859(03)00064-8

DO - 10.1016/S0198-8859(03)00064-8

M3 - Article

C2 - 12770795

AN - SCOPUS:12444304481

SN - 0198-8859

VL - 64

SP - 629

EP - 632

JO - Human Immunology

JF - Human Immunology

IS - 6

ER -

Lack of association of CCR2-64I and CCR5-Δ32 with type 1 diabetes and latent autoimmune diabetes in adults

Abstract

Keywords*

Field of Science*

Publication Type*

UN SDGs

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