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This article is part of the supplement: Proceedings of the 8th Global Arthritis Research Network (GARN) Meeting and 1st Bio-Rheumatology International Congress (BRIC)

Open Badges Poster presentation

Balb/c FasKO mice develop allergic blepharitis associated with hyper-production of IgE

Ayumi Fukuoka1*, Shizue Yumikura-Futatsugi2, Suzuka Takahashi13, Hirotaka Kazama1, Kenji Nakanishi2 and Shin Yonehara1

  • * Corresponding author: Ayumi Fukuoka

Author Affiliations

1 Graduate School of Biostudies, Kyoto University, Japan

2 Department of Immunology and Medical Zoology, Hyogo College of Medicine, Japan

3 Institute of Genome Reserch, The University of Tokushima, Japan

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Arthritis Research & Therapy 2012, 14(Suppl 1):P19  doi:10.1186/ar3620

The electronic version of this article is the complete one and can be found online at:

Published:9 February 2012

© 2012 Fukuoka et al.; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Poster presentation

Fas is a member of the TNF receptor family and crucial for induction of apoptosis. MRL- lpr/lpr mice, which carry a mutation of Fas, spontaneously develop systemic autoimmune disease including arthropathy, indicating that Fas plays an important role in elimination of self-reactive immunocytes by apoptosis. In addition to autoimmune diseases, we found a novel phenotype of FasKO mice exclusively in Balb/c genetic background that is allergic blepharitis. Allergic blepharitis is revealed in Balb/c FasKO mice from 15 week-old and about 85% of the mice suffered from allergic blepharitis at 35 week-old. Serum concentrations of both IgG1 and IgE Abs were about 100-times higher in 20-week old FasKO mice than in WT mice; however, there was no significant difference between WT and FasKO mice in the ability of B cells to produce IgG1 and IgE Abs in the presence of IL-4 and anti-CD40 Ab inducing co-stimulatory signals. Additionally, the production of IL-4 by T cells was same. These results suggested that other type of cells enhanced IgG1 and IgE Abs production from B cells in Balb/c FasKO mice. To identify the cells enhancing IgG1 and IgE Abs production, we cultured B cells in vitro in the presence of IL-4 and anti-CD40 Ab together with various types of cells from Balb/c FasKO mice. In the result, we found FasKO non-T non-B cells upregulated the production of both IgG1 and IgE from B cells. Moreover, the number of these cells was specifically increased in Balb/c FasKO mice.All the results indicate that these cells enhance production of IgG1 and IgE from B cells in the presence of IL-4 and anti-CD40 Ab, and excessive accumulation of these cells may cause allergy via hyper-production of IgE.

thumbnailFigure 1. Balb/c FasKO mice develope allergic blepharitis.


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