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More MS news articles for March 2003

Upregulation of b7 molecules (cd80 and cd86) and exacerbated eosinophilic pulmonary inflammatory response in mice lacking the ifn-beta gene

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12642836&dopt=Abstract

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.

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.