Th2 cytokine genotypes are associated with a milder form of primary Sjogren's syndrome.

Authors: Pertovaara, M  Antonen, J  Hurme, M 
Citation: Pertovaara M, etal., Ann Rheum Dis. 2006 May;65(5):666-70. Epub 2005 Sep 15.
Pubmed: (View Article at PubMed) PMID:16166103
DOI: Full-text: DOI:10.1136/ard.2005.040956

BACKGROUND: Immunohistological studies on salivary and lacrimal glands have yielded conflicting results on the Th1/Th2 balance in primary Sjogren's syndrome (pSS). OBJECTIVE: To establish whether pSS is a Th1 or Th2 directed autoimmune disease by analysing the polymorphism of the genes encoding for cytokines involved in the regulation of Th1/Th2 differentiation. METHODS: The polymorphisms of the genes encoding for interleukin 4 (IL4) -590 C/T, interleukin 13 (IL13) +2044 G/A, and interferon gamma (IFNG) +874 T/A were analysed in 63 white Finnish patients with pSS (61 female, two male) and in 63 healthy controls. The clinical and immunological data on the pSS patients were analysed in relation to these cytokine gene polymorphisms. RESULTS: There were no significant differences in the genotype or allele frequencies of IL4 -590, IL13 +2044, or IFNG +874 between pSS patients and controls. The erythrocyte sedimentation rate and concentrations of serum IgA and serum beta2 microglobulin were lower in pSS patients carrying the IL4 -590 T allele or the IL13 +2044 A allele than in those not carrying the respective alleles. The IL4 -509 T allele and IL13 +2044 A allele carriers less often had purpura than the corresponding non-carriers. CONCLUSIONS: The frequencies of the cytokine genotypes regulating Th1/Th2 differentiation did not differ between pSS patients and controls. However, the presence of cytokine genotypes with increased susceptibility to atopic and other Th2 diseases was associated with signs of a milder form of pSS. This finding would favour a hypothesis envisaging pSS as primarily a Th1 mediated autoimmune disease.

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CRRD ID: 11528572
Created: 2016-08-16
Species: All species
Last Modified: 2016-08-16
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.