Innate and neuro-immune control of allergic immunity
The innate immune system plays a central role in adaptive immune initiation by sensing microbial invasion and environmental stress and using that information to promote specific adaptive immune outcomes. But how does the innate immune system do this? In the case of Type-1 immunity, generally regarded as the responses against bacteria and viruses, dendritic cells in the periphery are activated through their pattern recognition receptors by microbial pathogen associated molecular patterns. This leads to dendritic cell maturation, which is characterized by increased antigen presentation, upregulation of costimulatory molecules, migration to the draining lymph node, and secretion of cytokines involved in T helper cell skewing. But these paradigms may not underlie allergic, or Type-2, immune responses. Type-2 immunogens are able to induce dendritic cell migration and maturation in vivo, but not in vitro. And although dendritic cells are necessary for Th2 differentiation they are not sufficient. These observations indicate that different pathways may promote the innate immune sensing of Type-2 immunogens such as allergens and venoms. Furthermore, they illustrate a possible role for accessory cells in the initiation of Type-2 immunity.
Using the tools of cellular immunology, my laboratory seeks to elucidate the cellular and molecular mechanisms behind the innate immune control of allergic disease. We study the ways that allergens and venoms are sensed by the body via both immune cells and sensory neurons, and how this sensing leads to innate immune activation. Furthermore, with the goal of identifying novel therapeutics to treat allergic inflammatory disorders, we are interested in identifying novel accessory cells and signals involved in Th2-differentiation in both mice and men.
Center for Immunology and Inflammatory Diseases
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