|Le Gros, Graham|
Submitted to: Journal of Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/8/2007
Publication Date: 8/15/2007
Citation: Shen, T., Wang, L., Kim, S., Lantz, C., Urban Jr, J.F., Le Gros, G., Min, B. 2007. T cell IL-3 production is critical for parasite infection-induced basophil production, as well as basaphil survival in vitro, yet in vivo basophil survival is IL-3 independent. Journal of Immunology. July 15. epub ahead of print. Interpretive Summary: Probiotic bacteria are living microorganisms that, when added to foods or dietary supplements in sufficient number, can generally benefit health. They have been used to reduce the incidence of allergic diseases in targeted populations with a disposition to express allergy. The ability to monitor allergic expression is often reserved to clinical manifestation of a response to the allergen, but use of peripheral blood cells has the advantage of easy access and does not require exposure of the patient to the allergen. One of the major cell populations in the peripheral blood that respond to allergens is the basophil. It is in relatively low numbers in the blood, and the features that control development of these cells are not well known. The current study used a mouse model to examine key regulatory elements that induce basophil differentiation during a parasite infection which is used to model the characteristics of allergic disease. It was found that IL-3 is a protein messenger molecule that controls basophil survival in cell cultures, but it is only one of several such molecules that control survival in the animal. These results suggest that the basophil is responsive to immune stimulation that is associated with the signals that activate it to respond to allergens. This information would benefit research to ameliorate the expression of food allergies in humans since the basophil contributes to expression of the disease.
Technical Abstract: Enhanced basophil production is often associated with Th2-related conditions such as parasite infections or allergic inflammations. Our previous study demonstrated that T cell activation is necessary to promote basophil production in Nippostrongylus brasiliensis (Nb)-infected mice. Yet, mechanisms underlying T cell-mediated basophil responses are less clear. In this report, it was shown that IL-3 produced by activated T cells enhances basophil production in Nb infected mice. IL-3-deficient mice or Rag2-/- recipients of IL-3-deficient T cells failed to support basophil production following the Nb infection. Interestingly, although IL-3 was critical for preventing basophil apoptosis in vitro, IL-3 had little or no role in basophil survival in vivo. Collectively, these results highlight a novel mechanism by which activation of adaptive immune components induces production of basophils via IL-3 production.