The goal of these studies is to establish an understanding of the signals which regulate gene expression of the low affinity receptor for IgE (CD23 Or FCepsilonRII). Our hypothesis is that there is enhanced expression of CD23 in occupational/environmental asthma. The late response and chronic inflammation in asthma may involve the cell types and cytokines known to either express or to regulate CD23 gene expression. In order to establish whether CD23 is a biomarker for asthma we will determine the correlation between CD23 gene expression and disease in patients with atopic asthma compared to normal controls. In population-based studies, we will determine if changes in CD23 levels indicate susceptibility to developing asthma. At the cellular level, we will analyze the function of CD23+ T cells and at the molecular level, we will identify the DNA regulatory elements for CD23 expression in T cells. The ultimate goal of these studies is to determine what role this receptor may play in the development of asthma and to devise intervention strategies to prevent asthma. This proposal is unique in integrating the disciplines of molecular biology, cellular immunology, and clinical epidemiology in an effort to determine the mechanisms and potential interventions for occupational/ environmental asthma.
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| Cernadas, M; De Sanctis, G T; Krinzman, S J et al. (1999) CD23 and allergic pulmonary inflammation: potential role as an inhibitor. Am J Respir Cell Mol Biol 20:1-8 |
| Lara-Marquez, M L; Deykin, A; Krinzman, S et al. (1998) Analysis of T-cell activation after bronchial allergen challenge in patients with atopic asthma. J Allergy Clin Immunol 101:699-708 |
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| Krinzman, S J; De Sanctis, G T; Cernadas, M et al. (1996) T cell activation in a murine model of asthma. Am J Physiol 271:L476-83 |
