Background

The prevalence of food allergy is rising and etiologic factors remain uncertain. Evidence implicates a role of vitamin D in the development of atopic diseases. Based on seasonal patterns of UVB exposure (and consequent vitamin D status), we hypothesized that food allergy patients are more often born in fall or winter.

Objective

Investigate whether season of birth is associated with food allergy.

Methods

We performed a multicenter chart review of all patients presenting to three Boston emergency departments (EDs) for food-related acute allergic reactions between 1/1/01 and 12/31/06. Months of birth among food allergy patients were compared to those of patients visiting the ED for reasons other than food allergy.

Results

We studied 1,002 food allergy patients. Among younger children with food allergy (age <5 years) – but not among older children or adults – 41% were born in spring/summer compared to 59% in fall/winter (P=0.002). This approximately 40/60 ratio differed from birth season of children treated in the ED for non-food allergy reasons (P=0.002). Children <5 years old born in fall/winter had a 53% higher odds of food allergy compared to controls. This finding was independent of the suspected triggering food and allergic comorbidities.

Conclusions

Food allergy is more common in Boston children who were born in the fall and winter seasons. We propose that these findings are mediated by seasonal differences in UVB exposure. These results add support to the hypothesis that seasonal fluctuations in sunlight and perhaps vitamin D may be involved in the pathogenesis of food allergy.

TFIID is a multiprotein complex consisting of the TATA box binding protein and multiple tightly associated proteins (TAFIIs) that are required for transcription by selected activators. We previously reported cloning and partial characterization of human TAFII130 (hTAFII130). The central domain of hTAFII130 contains four glutamine-rich regions, designated Q1 to Q4, that are involved in interactions with the transcriptional activator Sp1. Mutational analysis has revealed specific regions within the glutamine-rich (Q1 to Q4) central region of hTAFII130 that are required for interaction with distinct activation domains. We tested amino- and carboxyl-terminal deletions of hTAFII130 for interaction with Sp1 activation domains A and B (Sp1A and Sp1B) and the N-terminal activation domain of CREB (CREB-N) by using the yeast two-hybrid system. Our results indicate that Sp1B interacts almost exclusively with the Q1 region of hTAFII130. In contrast, Sp1A makes multiple contacts with Q1 to Q4 of hTAFII130, while CREB-N interacts primarily with the Q1-Q2 hTAFII130 subdomain. Consistent with these interaction studies, overexpression of the Q1-to-Q4 region in HeLa cells inhibits Sp1- but not VP16-mediated transcriptional activation. These findings indicate that the Q1-to-Q4 region of hTAFII130 is required for Sp1-mediated transcriptional enhancement in mammalian cells and that different activation domains target distinct subdomains of hTAFII130.