Hizawa N, Freidhoff L R, Ehrlich E, Chiu Y F, Duffy D L, Schou C, Dunston G M, Beaty T H, Marsh D G, Barnes K C, Huang S K
Division of Clinical Immunology, The Johns Hopkins Asthma & Allergy Center, Baltimore, MD 21224, USA.
J Allergy Clin Immunol. 1998 Sep;102(3):449-53. doi: 10.1016/s0091-6749(98)70134-4.
We have recently conducted a genome-wide screening for genes influencing Dermatophagoides pteronyssinus-specific IgE responsiveness as a part of the Collaborative Study on the Genetics of Asthma (CSGA), which showed evidence for linkage in some regions, including chromosomes 5131-q33 and 11q13 in African American families.
To clarify relative contributions of these regions to atopy in the same African American population, we have conducted further genetic linkage studies of specific IgE responses toward common inhaled allergens.
We studied 328 individuals in 58 African American families participating in the CSGA. Specific IgE responses toward Dermatophagoides farinae, cat, dog, American cockroach, rye grass, and Bermuda grass, as measured by skin tests, were used for multipoint linkage analysis with polymorphic markers on chromosomes 5q31-q33 and 11q13.
Specific IgE response toward American cockroach showed evidence for linkage to chromosomes 5q31-q33 (P = .0050) and 11q13 (P = .017). Specific IgE response toward dog showed evidence for linkage with chromosome 5q31-q33 (P = .0043). Evidence for linkage with chromosome 11q13 was obtained for specific IgE responses toward Dermatophagoides farinae (P = .012), cat (P = .035), and Bermuda grass (P = .017). The presence of a positive ST response for at least 1 of 30 common allergens showed evidence for linkage to chromosomes 5q31-q33 (P = .017) and 11q13 (P = .00058).
These data support that genes on both chromosomes 5q31-q33 and 11q13 confer susceptibility to upregulated IgE-mediated immune responses in this African American population. The putative genes on chromosomes 5q31-q33 and 11q13, however, showed contrasting effects on atopy, which may result from strong gene-environmental interactions.
作为哮喘遗传学合作研究（CSGA）的一部分，我们最近进行了一项全基因组筛查，以寻找影响户尘螨特异性IgE反应性的基因，研究结果显示在某些区域存在连锁证据，包括非裔美国家庭中的5号染色体131-q33区域和11号染色体11q13区域。
为了阐明这些区域对同一非裔美国人群特应性的相对贡献，我们针对常见吸入性过敏原的特异性IgE反应进行了进一步的遗传连锁研究。
我们研究了参与CSGA的58个非裔美国家庭中的328名个体。通过皮肤试验测量的针对粉尘螨、猫、狗、美洲大蠊、黑麦草和百慕大草的特异性IgE反应，用于与5号染色体q31-q33和11号染色体11q13上的多态性标记进行多点连锁分析。
针对美洲大蠊的特异性IgE反应显示与5号染色体q31-q33（P = 0.0050）和11号染色体11q13（P = 0.017）存在连锁证据。针对狗的特异性IgE反应显示与5号染色体q31-q33（P = 0.0043）存在连锁证据。针对粉尘螨（P = 0.012）、猫（P = 0.035）和百慕大草（P = 0.017）的特异性IgE反应获得了与11号染色体11q13连锁的证据。对30种常见过敏原中至少1种呈阳性皮肤试验反应显示与5号染色体q31-q33（P = 0.017）和11号染色体11q13（P = 0.00058）存在连锁证据。
这些数据支持5号染色体q31-q33和11号染色体11q13上的基因均使该非裔美国人群易发生IgE介导的免疫反应上调。然而，5号染色体q31-q33和11号染色体11q13上的推定基因对特应性表现出相反的作用，这可能是由强烈的基因-环境相互作用导致的。
