This work was supported by grants from the National Health and Medical Research Council of Australia, and the Netherlands Organization for Scientific Research (Grant: R93–183).
Regulation of IgE production in pre-sensitized animals: in vivo elimination of alveolar macrophages preferentially increases IgE responses to inhaled allergen*
Article first published online: 27 APR 2006
Clinical & Experimental Allergy
Volume 22, Issue 12, pages 1107–1114, December 1992
How to Cite
THEPEN, T., McMENAMIN, C., GIRN, B., KRAAL, G. and HOLT, P. G. (1992), Regulation of IgE production in pre-sensitized animals: in vivo elimination of alveolar macrophages preferentially increases IgE responses to inhaled allergen. Clinical & Experimental Allergy, 22: 1107–1114. doi: 10.1111/j.1365-2222.1992.tb00137.x
- Issue published online: 27 APR 2006
- Article first published online: 27 APR 2006
- Submitted 16 September 1991; revised 27 April 1992; accepted 7 May 1992.
Intratracheal inoculation of dichloromethylene diphosphonate encapsulated in liposomes leads to the rapid accumulation of this drug in alveolar macrophage (AM) phagolysosomes, and the death of the majority of these cells over the ensuing 24–48 hr. The technique is highly selective for phagocytes and has no detectable side-effects on other cells in the lung. The present experiments demonstrate that following AM depletion, pre-sensitized animals respond to aerosol challenge via secondary serum IgE (but not IgG) responses, and the accumulation of large numbers of allergen-specific and non-specific antibody forming cells in respiratory tract regional lymph nodes and in lung and airway tissues; the latter comprise both IgE and IgG plasma cells, which were detected in the approximate ratio of 2.5:1. Moreover, aerosol challenged AM-depleted animals develop large mononuclear cell infiltrates in the lung and airways, which includes a substantial CD4+ T-cell component. These results suggest a major role for AM in regulating the magnitude of secondary IgE responses to inhaled allergen.