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CCR 5‐ D elta32: implications in SLE development
Author(s) -
Carvalho C.,
Calvisi S. L.,
Leal B.,
Bettencourt A.,
Marinho A.,
Almeida I.,
Farinha F.,
Costa P. P.,
Silva B. M.,
Vasconcelos C.
Publication year - 2014
Publication title -
international journal of immunogenetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.41
H-Index - 47
eISSN - 1744-313X
pISSN - 1744-3121
DOI - 10.1111/iji.12094
Subject(s) - chemokine , immunology , allele , pathogenesis , heterozygote advantage , chemokine receptor , disease , receptor , autoimmunity , autoimmune disease , medicine , biology , inflammation , gene , immune system , antibody , genetics
Summary Systemic lupus erythematosus ( SLE ) is a prototypical autoimmune disease with strong genetic and environmental components. Previous studies have shown increased levels of several chemokines in active SLE . C‐C chemokine receptor type 5 ( CCR 5) is involved in the recruitment of inflammatory cells into tissues, and mechanisms modulating CCR 5 expression and function may interfere in SLE development, influencing the clinical course of the disease. The aim of this study was to evaluate the possible association between the CCR 5∆32 base‐pair deletion polymorphism and SLE disease in a group of Portuguese patients. A total of 219 patients with SLE and 205 healthy individuals were studied. The frequency of CCR 5/∆32 heterozygotes was lower in patients with SLE than in controls (8% vs. 15% OR = 0.5162; P = 0.0319), suggesting a protective association between CCR 5∆32 allele and SLE . These results highlight the protective role of Th1 cells that express CCR 5 in SLE pathogenesis.
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