BACKGROUND: The role of interleukin (IL)-29 in innate immunity has been recognized recently, and it is regarded as a potent bioactive molecule. However, little is known about its role in the pathogenesis of allergy. Because mast cells are recognized as primary effector cells of allergy, we investigated the potential relationship between IL-29 and mast cells in this study. OBJECTIVE: To examine the expression of IL-29 in mast cells and the influence of IL-29 on mast cell mediator release and accumulation. METHODS: Expression of IL-29 in mast cells was determined by double-labeling immunohistochemistry and flow cytometry analysis. Mast cell cell-line was cultured to examine the mediator release, and mouse peritoneal model was employed to observe the mast cell accumulation. RESULTS: Large proportions of mast cells expressing IL-29 were localized in human tissue including the colon, tonsil and lung. Mast cells can release substantial quantity of IL-29 upon challenge with proteolytic allergens. Extrinsic IL-29 provoked IL-4 and IL-13 release from mast cell line P815 cells through PI3K/Akt and (JAK)/STAT3 signaling pathways, but failed to induce mast cell histamine release from human mast cells. Extrinsic IL-29 also induced mast cell infiltration in mouse peritoneum by a CD18- and ICAM1-dependent mechanism. CONCLUSION: Mast cell-derived IL-29 has the potential to be involved in the pathogenesis of allergic inflammation.
BACKGROUND: The role of interleukin (IL)-29 in innate immunity has been recognized recently, and it is regarded as a potent bioactive molecule. However, little is known about its role in the pathogenesis of allergy. Because mast cells are recognized as primary effector cells of allergy, we investigated the potential relationship between IL-29 and mast cells in this study. OBJECTIVE: To examine the expression of IL-29 in mast cells and the influence of IL-29 on mast cell mediator release and accumulation. METHODS: Expression of IL-29 in mast cells was determined by double-labeling immunohistochemistry and flow cytometry analysis. Mast cell cell-line was cultured to examine the mediator release, and mouse peritoneal model was employed to observe the mast cell accumulation. RESULTS: Large proportions of mast cells expressing IL-29 were localized in human tissue including the colon, tonsil and lung. Mast cells can release substantial quantity of IL-29 upon challenge with proteolytic allergens. Extrinsic IL-29 provoked IL-4 and IL-13 release from mast cell line P815 cells through PI3K/Akt and (JAK)/STAT3 signaling pathways, but failed to induce mast cell histamine release from human mast cells. Extrinsic IL-29 also induced mast cell infiltration in mouse peritoneum by a CD18- and ICAM1-dependent mechanism. CONCLUSION: Mast cell-derived IL-29 has the potential to be involved in the pathogenesis of allergic inflammation.