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CD14: a bridge between innate immunity and adaptive IgE responses

Respiratory Sciences Center University of Arizona, Tucson, Arizona, USA, Departments of Cell Biology and Anatomy, University of Arizona, Tucson, Arizona, USA, donata{at}resp-sci.arizona.edu

Mauro Baldini

Respiratory Sciences Center University of Arizona, Tucson, Arizona, USA

Debra Stern

Respiratory Sciences Center University of Arizona, Tucson, Arizona, USA

I. Carla Lohman

Respiratory Sciences Center University of Arizona, Tucson, Arizona, USA

Marilyn Halonen

Respiratory Sciences Center University of Arizona, Tucson, Arizona, USA, Department of Pharmacology, Immunology, University of Arizona, Tucson, Arizona, USA

Fernando Martinez

Respiratory Sciences Center University of Arizona, Tucson, Arizona, USA, Department of Pediatrics, College of Medicine, University of Arizona, Tucson, Arizona, USA

Total IgE levels are known to be under genetic control. Linkage studies have indicated that one or more loci on chromosome 5q may control total IgE, as well as asthma and bronchial hyper-responsiveness to non-specific stimuli. Our group has undertaken a systematic analysis of chromosome 5q, and has recently characterized five single nucleotide polymorphisms at position —1619, —1359, —1145, —809, and —159 in the promoter of the gene encoding CD14, the myeloid pattern recognition receptor that is critical for efficient innate immune responses to lipopolysaccharide and bacterial ligands. Individuals homozygous for the three major CD14 haplotypes found in the Children Respiratory Study population (n = 390) were analyzed for serum levels of total IgE and soluble CD14. A strong inverse correlation was found between these two parameters, i.e. carriers of the —1359T/—1145A/—159C haplotype had the highest levels of IgE, and the lowest levels of sCD14. Conversely, carriers of the —1359G/—1145G/—159T haplotype had the highest levels of sCD14 and the lowest IgE values. Our results suggest that genetic variation in CD14, a key gene of innate immunity, may modulate the effects that exposure to bacterial ligands has on the development of Th2 responses.

Journal of Endotoxin Research, Vol. 7, No. 1, 45-48 (2001)
DOI: 10.1177/09680519010070010701


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