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Background: The T-cell immunoglobulin domain and mucin domain (TIM) gene family and the gene for IL-2–inducible T-cell kinase (ITK), located in chromosome 5q33 and potentially involved in the T-cell proliferation and differentiation, are good candidate genes for allergic diseases. Objective: We assessed the role of polymorphisms in the TIM family genes and ITK in atopy, eczema, and asthma. Methods: Twenty-one polymorphisms in the TIM-ITK gene cluster were genotyped in 564 children enrolled in the Tucson Children''s Respiratory Study. Skin prick tests to common allergens were performed at age 6.1 years (n=508), age 10.8 years (n=539), and age 16.6 years (n=424). Asthma and eczema were assessed by questionnaire at these 3 points. Averaged relative risks were estimated. Results: One 15-bp insertion/deletion in exon 4 of TIM1 was significantly related to atopy and eczema (relative risk associated with carrying at least 1 rare allele=1.24 [1.07-1.45], P =.005; and 1.43 [1.01-2.01], P =.004, respectively). The 3 tested single nucleotide polymorphisms (SNPs) in TIM3 were significantly related to atopy and eczema. One of them, at position +4259 calculated from the translation start site, predicts a putative change in the amino acid sequence of the protein, and was the most strongly related to atopy (relative risk=1.28 [1.12-1.47]; P =.0003). SNPs in the 5′ genomic region in ITK, which show moderate linkage disequilibrium with those in TIM3, had an independent effect on atopy. None of the polymorphisms studied was related to asthma. Conclusion: Our findings support a potential role for SNPs in TIM1, TIM3, and ITK, independent of each other, in allergic diseases. [Copyright &y& Elsevier]

This article cites a study which was aimed to determine whether the polymorphisms at codons 16 and 27 of the β2-adrenoceptor are significant predictors of the persistence of asthma during adolescence. Population-based longitudinal cohort studies, reportedly, have consistently shown that severity and frequency of asthma symptoms are among the strongest predictors for the persistence of asthma from childhood to adulthood. The children included in this study are a subset from the large birth cohort of the Tucson Children's Respiratory Study. Detailed information on the design and the enrollment process of this study has been provided elsewhere. Briefly, between May 1980 and October 1984, parents planning to use the pediatricians of a health maintenance organization in Tucson, Arizona, were contacted shortly after their child was born, and a total of 1,246 healthy infants were enrolled in the study. This study provides evidence for a strong gender-specific effect of the Gly16 polymorphism on the persistence of asthma after the onset of puberty.