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J Allergy Clin Immunol. 1999 Sep;104(3 Pt 1):575-84.

Altered expression and action of the low-affinity IgE receptor FcepsilonRII (CD23) in asthmatic airway smooth muscle.

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  • 1Divisions of Pulmonary Medicine and Allergy, Immunology, and Infectious Diseases, Joseph Stokes, Jr Research Institute, Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.



Changes in cell surface expression of certain immunoglobulin Fc receptors have been demonstrated in leukocytes isolated from the lungs of atopic asthmatic individuals. This, together with emerging evidence that Fc receptors can also be expressed and activated in non-bone marrow-derived cell types, including airway smooth muscle (ASM), raises the hypothesis that the atopic asthmatic ASM phenotype is associated with an altered endogenous expression and action of specific Fc receptors present in the ASM itself.


The current study addressed the above hypothesis by examining (1) whether the expression of certain key Fc receptor subtypes for IgE and IgG is altered in ASM tissue isolated from human atopic asthmatic individuals and (2) whether this altered Fc receptor expression is comparably induced in naive human ASM tissue and cultured cells after their passive sensitization with human atopic asthmatic serum or IgE immune complexes.


Messenger RNA and cell surface protein expression of the individual IgG receptor subtypes FcgammaRI, FcgammaRII, and FcgammaRIII, as well as the IgE receptor subtypes FcepsilonRI and FcepsilonRII, were examined in human ASM tissue isolated from atopic asthmatic and control (nonatopic/nonasthmatic) individuals. In addition, we examined the effects of passive sensitization of ASM tissue and cultured ASM cells with control serum, atopic asthmatic serum, or exogenously administered IgE immune complexes on Fc receptor expression and action (ie, induction of proinflammatory cytokine release).


The observations demonstrate that (1) human ASM tissue expresses messenger RNA and surface protein for FcepsilonRII, as well as for all the Fcgamma receptor subtypes, (2) in contrast to unaltered Fcgamma subtype expression, however, relative to control human ASM, FcepsilonRII is significantly up-regulated in inherently asthmatic ASM tissue, (3) up-regulated expression of FcepsilonRII represents, at least in part, an inducible phenomenon that is largely attributed to IgE immune complex-coupled activation of the receptor, and (4) the latter action is associated with FcepsilonRII-induced autologous elaboration of the proinflammatory cytokine, IL-1beta, by the atopic sensitized ASM.


These observations provide new evidence that human ASM tissue expresses FcepsilonRII in addition to all 3 subtypes of Fcgamma receptors and that the expression of FcepsilonRII is selectively increased in atopic asthmatic ASM, a phenomenon associated with IgE immune complex/FcepsilonRII-mediated elaboration of IL-1beta by the ASM itself.

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