Co-operation between humoral and cellular immunity in pulmonary lung inflammation

Abstract

Asthma is a respiratory disease, characterized by elevated serum immunoglobulin E (IgE) levels, chronic eosinophilic airway inflammation, and airway hyperresponsiveness (AHR). In vivo studies have shown that interleukin4 (IL-4), IL-5, and IL-13 are involved in allergic asthma development. The role of T lymphocytes in asthma has been extensively studied but the role of IgE in asthma is not well understood. It was recently shown that IgE is able to induce activation of T cells in the presence of antigen in vivo. Therefore we hypothesize that the role of IgE is in aiding the response elicted by CD4 Th2 cells during asthma. Using an IgE passive sensitization model together with the adoptive transfer model, we have shown that there was no recruitment of eosinophils in the airways or antigen specific T cells in the lungs when mice were given both antigen-specific IgE and polarized Th2 cells.