IL-13 Regulates the Immune Response to Inhaled Antigens
| Autor: | Kaushik Parthasarathi, Kesha Robinson, Debra D. Donaldson, Gabriele Grunig, Viswanath P. Kurup, Andrew Neil James Mckenzie, Eleen Daley, Anthony Chow, Thomas Tschernig, Jocelyn Padilla |
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| Rok vydání: | 2005 |
| Předmět: |
Ovalbumin
Immunology Antigen presentation Priming (immunology) CD11c Mice Transgenic chemical and pharmacologic phenomena Immunophenotyping Mice Immune system Antigen Administration Inhalation Animals Immunology and Allergy Antigens Lung Administration Intranasal Cells Cultured Mice Knockout Mice Inbred BALB C MHC class II Interleukin-13 CD40 biology Dendritic Cells Allergens CD11c Antigen Mice Inbred C57BL Interleukin 13 biology.protein Inflammation Mediators Bronchoalveolar Lavage Fluid Signal Transduction |
| Zdroj: | The Journal of Immunology. 174:8097-8105 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.174.12.8097 |
| Popis: | The large inhibitory effect of IL-13 blockers on the asthma phenotype prompted us to ask whether IL-13 would play a role in regulating the allergic immune response in addition to its documented effects on structural pulmonary cells. Because IL-13 does not interact with murine T or B cells, but with monocytes, macrophages, and dendritic cells (DCs), we examined the role of IL-13 in the activation of pulmonary macrophages and DCs and in the priming of an immune response to a harmless, inhaled Ag. We found that a majority of cells called “alveolar or interstitial macrophages” express CD11c at high levels (CD11chigh) and are a mixture of at least two cell types as follows: 1) cells of a mixed phenotype expressing DC and macrophage markers (CD11c, CD205, and F4/80) but little MHC class II (MHC II); and 2) DC-like cells expressing CD11c, CD205, MHC II, and costimulatory molecules. Endogenous IL-13 was necessary to induce and sustain the increase in MHC II and CD40 expression by pulmonary CD11chigh cells, demonstrated by giving an IL-13 inhibitor as a measure of prevention or reversal to allergen-primed and -challenged mice. Conversely, IL-13 given by inhalation to naive mice increased the expression of MHC II and costimulatory molecules by CD11chigh cells in an IL-4Rα-dependent manner. We found that exogenous IL-13 exaggerated the immune and inflammatory responses to an inhaled, harmless Ag, whereas endogenous IL-13 was necessary for the priming of naive mice with an inhaled, harmless Ag. These data indicate that blockade of IL-13 may have therapeutic potential for controlling the immune response to inhaled Ags. |
| Databáze: | OpenAIRE |
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