Critical role of CD23 in allergen-induced bronchoconstriction in a murine model of allergic asthma

Abstract

CD23‐deficient and anti‐CD23 monoclonal antibody‐treated mice were used to investigate the role of the low‐affinity receptor for IgE (CD23) in allergic airway inflammation and airway hyperresponsiveness (AHR). While there were no significant differences in ovalbumin (OVA)‐specific IgE titers and tissue eosinophilia, evaluation of lung function demonstrated that CD23− / − mice showed an increased AHR to methacholine (MCh) when compared to wild‐type mice but were completely resistant to the OVA challenge. Anti‐CD23 Fab fragment treatment of wild‐type mice did not affect the MCh‐induced AHR but significantly reduced the OVA‐induced airway constriction. These results imply a novel role for CD23 in lung inflammation and suggest that anti‐CD23 Fab fragment treatment may be of therapeutic use in allergic asthma.

How antibodies act as natural adjuvants

“…However, in the western world it is more likely to be involved in the development of allergic disease [98,99]. Support for a role for IgE-mediated antigen presentation in allergy comes from animal studies [100,101] and studies on patient material [92,102,103].…”

Polymorphism R62W results in resistance of CD23 to enzymatic cleavage in cultured cells

“…Anti-CD23 antibodies also can reduce allergic airway inflammation including IgE levels and eosinophilia, and normalize allergen-stimulated airway responsiveness in wild-type sensitized mice. 18,19 Recent studies also indicate that genetic polymorphisms of CD23 as well as its expression levels are important factors for the occurrence, severity and even treatment in allergic diseases. A significant allele and haplotype association of CD23 with the phenotypes in allergic diseases has been observed in a genetic epidemiological study.…”

Mast Cells and Company

“…Various strategies that interfere with eosinophil recruitment, activation, and survival have been proven successful in animal models of experimental asthma. These strategies included inhibition of eosinophil recruitment and activation by targeting IL-5 (Foster et al, 1996; Yoshida et al, 1996; Lee et al, 1997), CD131 (Nicola et al, 1996; Sun et al, 1999), CD300a (Munitz et al, 2006), CD23 (Dasic et al, 1999; Haczku et al, 2000), CD48 (Munitz et al, 2007), CCR-3 (Pope et al, 2005; Wegmann et al, 2007), or PGD2 signaling (Sugimoto et al, 2003; Uller et al, 2007; Shichijo et al, 2009; Stearns et al, 2009). Other strategies aimed at reducing eosinophil numbers by using mAbs anti-CCR-3 (Justice et al, 2003) or mAbs anti-Siglec F (Song et al, 2009).…”