6533b86cfe1ef96bd12c8bf7

RESEARCH PRODUCT

Epidermal Cells Enhance Interleukin 4 and Immunoglobulin E Production After Stimulation with Protein Allergen

subject

description

Exposure to certain allergens via epithelial tissues is the primary route for tile induction of immunoglobulin E–dependent allergies of the immediate type associated with atopic diseases. In order to address the question whether and how epithelial cells might contribute to the induction or increase of T H2 -dependent IgE production, we performed co-culture experiments of syngeneic epidermal cells and cells from the associated lymphoid tissue or spleen (responder cells) of BALB/c mice primed with ovalbumin in vivo . In the presence of ovalbumin in vitro , immunoglobulin E but not immunoglobulin G 2a production was significantly enhanced by the addition of epidermal cells, and separation of epidermal cells from responder cells by a membrane that prevented cellular contacts or addition of antibodies against intercellular adhesion molecule–1 reduced the enhancement of immunoglobulin E production induced by epidermal cells. Depletion of major histocompatability complex class II + antigen presenting Langerhans cells from the epidermal cells prior to co-culture also reduced the enhancement of immunoglobulin E production induced by epidermal cells. The enhanced immunoglobulin E production was dependent on the induction of T H2 cell–derived interleukin-4 detected in co-cultures because it was completely inhibited after addition of anti–interleukin-4 antibodies that also lead to increased immunoglobulin G 2a production. Whereas interlukin-4 as not produced by epidermal cells, interleukin-4 was not produced by epidermal cells, interleukin-10 seemed to be one important mediator contributed by epidermal cells. Interleukin-10 skewed he response toward a T H2 -mediated IgE response because antibodies against interleukin-10 inhibited interleukin-4 and immunoglobulin E production, whereas they enhanced interferon- γ and immunoglobulin G 2a production.