Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Journal of Allergy and Clinical Immunology |
| Vol/bind | 111 |
| Udgave nummer | 3 |
| Sider (fra-til) | 550-7 |
| Antal sider | 7 |
| ISSN | 0091-6749 |
| Status | Udgivet - 2003 |
Bibliografisk note
Keywords: Animals; Antigens, CD; Antigens, CD80; Antigens, CD86; Blood Cells; Bronchoalveolar Lavage Fluid; Epitopes; Immune System; Immunoglobulin E; Interferon-beta; Interleukins; Membrane Glycoproteins; Mice; Mice, Knockout; Ovalbumin; Pulmonary Eosinophilia; Th2 Cells; Up-RegulationCitationsformater
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I: Journal of Allergy and Clinical Immunology, Bind 111, Nr. 3, 2003, s. 550-7.
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Upregulation of B7 molecules (CD80 and CD86) and exacerbated eosinophilic pulmonary inflammatory response in mice lacking the IFN-beta gene.
AU - Matheu, Victor
AU - Treschow, Alexandra
AU - Navikas, Vaidrius
AU - Issazadeh-Navikas, Shohreh
N1 - Keywords: Animals; Antigens, CD; Antigens, CD80; Antigens, CD86; Blood Cells; Bronchoalveolar Lavage Fluid; Epitopes; Immune System; Immunoglobulin E; Interferon-beta; Interleukins; Membrane Glycoproteins; Mice; Mice, Knockout; Ovalbumin; Pulmonary Eosinophilia; Th2 Cells; Up-Regulation
PY - 2003
Y1 - 2003
N2 - BACKGROUND: IFN-beta has been shown to be effective as therapy for multiple sclerosis. Some reports attributed its beneficial effects to the capacity to induce a T(H)2 response. However, other studies have suggested that endogenous type I IFN might downregulate the allergic response in mice. OBJECTIVE: We sought to define the differential role of endogenous IFN-beta in controlling the development of allergic inflammation. METHODS: We assessed whether deletion of the gene encoding IFN-beta (IFNB) with knockout mice participated in the development of allergic response in ovalbumin (OVA)-sensitized and OVA-challenged mice. RESULTS: OVA-sensitized and OVA-challenged mice with lack of the IFNB gene had more severe pulmonary inflammation with increased lung local response, including IL-4, IL-5, IL-13, IgE, eosinophilia, and goblet cells, than their litter mates (IFN-beta+/-), whereas no differences were observed in regard to local levels of IFN-gamma. Moreover, systemic response with IgE production is also enhanced. Lack of IFN-beta also results in significantly higher antigen-specific T cells, with higher levels of IL-4, IL-5, and IL-13, whereas no significant differences in IFN-gamma response could be observed. We have also detected a higher ratio of CD4+/CD8+ T cells and increased expression of B7.1/B7.2 on B cells and antigen-presenting cells in IFNB knockout mice. CONCLUSIONS: These results demonstrate that IFN-beta plays an important role in immunoregulation of allergic response in mice. The stronger pulmonary inflammation could be a consequence of significantly expanded antigen-specific CD4+ T(H)2 cells as a result of efficient antigen presentation by antigen-presenting cells and hence increased production of IgE by B cells.
AB - BACKGROUND: IFN-beta has been shown to be effective as therapy for multiple sclerosis. Some reports attributed its beneficial effects to the capacity to induce a T(H)2 response. However, other studies have suggested that endogenous type I IFN might downregulate the allergic response in mice. OBJECTIVE: We sought to define the differential role of endogenous IFN-beta in controlling the development of allergic inflammation. METHODS: We assessed whether deletion of the gene encoding IFN-beta (IFNB) with knockout mice participated in the development of allergic response in ovalbumin (OVA)-sensitized and OVA-challenged mice. RESULTS: OVA-sensitized and OVA-challenged mice with lack of the IFNB gene had more severe pulmonary inflammation with increased lung local response, including IL-4, IL-5, IL-13, IgE, eosinophilia, and goblet cells, than their litter mates (IFN-beta+/-), whereas no differences were observed in regard to local levels of IFN-gamma. Moreover, systemic response with IgE production is also enhanced. Lack of IFN-beta also results in significantly higher antigen-specific T cells, with higher levels of IL-4, IL-5, and IL-13, whereas no significant differences in IFN-gamma response could be observed. We have also detected a higher ratio of CD4+/CD8+ T cells and increased expression of B7.1/B7.2 on B cells and antigen-presenting cells in IFNB knockout mice. CONCLUSIONS: These results demonstrate that IFN-beta plays an important role in immunoregulation of allergic response in mice. The stronger pulmonary inflammation could be a consequence of significantly expanded antigen-specific CD4+ T(H)2 cells as a result of efficient antigen presentation by antigen-presenting cells and hence increased production of IgE by B cells.
M3 - Journal article
C2 - 12642836
SN - 0091-6749
VL - 111
SP - 550
EP - 557
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
IS - 3
ER -