Journal article
Loss of STAT6 promotes autoimmune disease and atopy on a susceptible genetic background
M Lau, E Tsantikos, MJ Maxwell, DM Tarlinton, GP Anderson, ML Hibbs
Journal of Autoimmunity | Published : 2012
Abstract
Atopy and autoimmunity are usually considered opposed immunological manifestations. Lyn-/- mice develop lupus-like autoimmune disease yet have coexistent intrinsic allergic traits and are prone to severe, persistent asthma induced exogenously. Recently it has been proposed that the Th2 environment and IgE auto-Abs promotes autoimmune disease in Lyn-/- mice. To examine this apparent contradiction, we derived Lyn-/- mice with a null mutation in STAT6, a regulator of Th2 immunity that integrates signaling from the IL-4/IL-13 receptor complex. Atopy and spontaneous peritoneal eosinophilia, characteristic of Lyn-/- mice, were lost in young Lyn-/-STAT6-/- mice; however, autoimmune disease was mark..
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Funding Acknowledgements
We thank Prof Foster from University of Newcastle, Australia for STAT6<SUP>-/-</SUP> mice, Val Feakes, Cameron Nowell and Amanda Light for technical assistance and Animal Facility staff for animal husbandry. ML holds Melbourne International and Endeavour International Postgraduate Research Scholarships, ET was a recipient of an Australian Postgraduate Award, and MJM, DMT and MLH hold fellowships from NH&MRC Australia. This work was supported by the NH&MRC Australia and made possible through Victorian State Government Operational Infrastructure Support and the Australian Government NH&MRC Independent Research Institute Infrastructure Support Scheme.