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Immunogenetic Correlates for Chlamydia trachomatis–Associated Tubal Infertility

From the Departments of Obstetrics and Gynecology, University of Washington, Seattle, Washington; Departments of Obstetrics and Gynecology, University of Nairobi, Nairobi, Kenya; Puget Sound Blood Center, Seattle, Washington; and University of British Columbia Centre for Disease Control, Vancouver, British Columbia, Canada.

Address reprint requests to: Craig R. Cohen, MD, MPH, University of Washington, Department of Obstetrics and Gynecology, Box 356460, Seattle, WA 98195; E-mail: crcohen{at}u.washington.edu.

OBJECTIVE: To understand immunogenetic mechanisms of Chlamydia trachomatis infection and tubal scarring.

METHODS: We measured and compared previously significant human leukocyte antigen (HLA) class II DQ alleles, their linked DRB genes, and polymorphisms in selected cytokine genes (tumor necrosis factor -308 promoter; transforming growth factor ß1-10 and -25 codons; interleukin 10-1082, -819, and -592 promoters; interleukin 6-174 promoter; and interferon +874 codon 1) among Kenyan women with confirmed tubal infertility with and without C trachomatis microimmunofluorescence antibody.

RESULTS: Two class II alleles, HLA-DR1*1503 and DRB5*0101, were detected less commonly in C trachomatis microimmunofluorescence seropositive women than in C trachomatis microimmunofluorescence seronegative women with infertility (0% versus 20%; odds ratio [OR] 0.05; 95% confidence interval [CI] 0, 0.7, and 6% versus 26%; OR 0.2; 95% CI 0.02, 1.0, respectively). These alleles are commonly linked as a haplotype at the DRB locus. This finding could not be explained through linkage disequilibrium with the other studied HLA or cytokine genes.

CONCLUSION: These alleles may lead to an immunologically mediated mechanism of protection against C trachomatis infection and associated tubal damage, or alternatively increase risk for tubal scarring due to another cause.

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