J Allergy Clin Immunol 2003 Mar;111(3):550-7
Matheu V, Treschow A, Navikas V, Issazadeh-Navikas S.
Section for Medical Inflammation Research, Institute for Cell and Molecular Biology, Lund University, Lund.
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.
We sought to define the differential role of endogenous IFN-beta in controlling the development of allergic inflammation.
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.
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.
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.