Clin Exp Immunol. 2004 Feb; 135(2): 194-9.  Related Articles, Links  

Desferrioxamine modulates chemically induced T helper 2-mediated autoimmunity
in the rat.

Wu Z, Holwill SD, Oliveira DB.

Department of Cellular and Molecular Medicine, St George's Hospital Medical
School, London, UK.

A rise in interleukin (IL) 4-dependent immunoglobulin E (IgE) is a hallmark of
the mercuric chloride (HgCl2)-induced Th2-mediated autoimmune syndrome in the
Brown Norway (BN) rat, and one of the mediators in allergic asthma in human.
Oxidative stress, a potential factor related to the pathogenesis of allergy and
asthma, has been shown to up-regulate IL-4 in mast cells and predispose to
degranulation in vitro. However, it remains unknown whether
oxidative/antioxidative imbalance plays a role in this Th2-driven model of
autoimmunity in the rat. Here we show that administration of the
non-sulphydryl-containing antioxidant desferrioxamine i.p. and s.c. to BN rats
reduces HgCl2-enhanced IL-4 gene expression and inhibits HgCl2-induced
Th2-mediated autoimmunity. Desferrioxamine treatment suppresses significantly
IgE production and lymphoproliferation, and reduces tissue injury in the form
of caecal vasculitis in the HgCl2-induced autoimmune syndrome. These results
support a role for oxidative stress in the pathogenesis of the HgCl2-induced
Th2-dominated autoimmune syndrome. This finding might have implications for
understanding the mechanisms involved in Th2 cell responses as seen in allergy
and asthma and thereby aid the development of new therapeutic strategies for
these diseases.

PMID: 14738445 [PubMed - in process]

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