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. Author manuscript; available in PMC: 2013 Sep 30.
Published in final edited form as: Ann Rheum Dis. 2007 Oct 30;67(8):1076–1083. doi: 10.1136/ard.2007.078048

Table 1.

Overall and CCL3L1 gene dose–dependent effects of CCR5 haplotypes on risk of developing SLE.

Model, CCR5 haplotype, CCL3L1 gene dose OR (95% CI) P
Model 1 (N=1059)
 HHE 1.61 (1.25 – 2.07) <0.001
 HHG*2 2.57 (1.71 – 3.86) <0.001
 HHF*1 0.24 (0.05 – 1.10) 0.067

Model 2 (<2 CCL3L1 copies, N=235)
 HHG*2 3.03 (1.35 – 6.79) 0.007
 HHE 1.83 (1.06 – 3.15) 0.030
 HHD 4.24 (0.82 – 21.99) 0.086

Model 3 (2 CCL3L1 copies, N=428)
 HHE 1.94 (1.31 – 2.88) 0.001

Model 4 (>2 CCL3L1 copies, N=396)
 HHG*2 4.12 (1.79 – 9.41) 0.001
 HHF*2 0.64 (0.42 – 0.98) 0.042
*

Model 1, stepwise unconditional logistic regression analysis for association between possession of CCR5 haplotypes and SLE disease susceptibility before accounting for CCL3L1 gene dose; Models 2 to 4, indicate stepwise unconditional logistic regression for association of the CCR5 haplotypes in the context of different CCL3L1 gene dose strata (i.e., <2, 2 and >2 CCL3L1 copies). All stepwise regression models used a probability criterion of P < 0.1. CI, confidence interval; OR, odds ratio. N, number of subjects. The analysis is for the combined three cohorts of SLE.

HH, human haplogroup