A single intracheal dose of liposome-encapsuled dichloro-methylene-diphosphonate resulted in the elimination of alveolar macrophages (AM) from the lung, creating a model to study the in vivo role of AM in the pulmonary immune response. Using intratracheally administered trinitrophenyl-keyhole limpet hemocyanin (TNP-KLH), the kinetics of the response, the location and number of TNP-specific antibody-forming cells, and the different Ig classes of the antibodies produced were studied in AM-depleted animals. The results show that AM elimination has a dramatic effect on the pulmonary immune responses against TNP-KLH. An increase in APC in lung-associated lymph nodes and a prolongation of the response is found, as well as an introduction of APC in lung tissue. In both experimental groups, the majority of the TNP-specific antibodies produced was IgG, followed by IgA and IgE, while very few IgM antibodies could be detected. We conclude from these results that AM are likely to play a role in controlling the pulmonary immune response in a suppressive way, thereby limiting the possible damage caused by severe immune responses in lung tissue.
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1 August 1989
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August 01 1989
Alveolar macrophage elimination in vivo is associated with an increase in pulmonary immune response in mice.
T Thepen,
T Thepen
Department of Histology, Vrije Universiteit, Amsterdam, The Netherlands.
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N Van Rooijen,
N Van Rooijen
Department of Histology, Vrije Universiteit, Amsterdam, The Netherlands.
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G Kraal
G Kraal
Department of Histology, Vrije Universiteit, Amsterdam, The Netherlands.
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T Thepen
Department of Histology, Vrije Universiteit, Amsterdam, The Netherlands.
N Van Rooijen
Department of Histology, Vrije Universiteit, Amsterdam, The Netherlands.
G Kraal
Department of Histology, Vrije Universiteit, Amsterdam, The Netherlands.
Online ISSN: 1540-9538
Print ISSN: 0022-1007
J Exp Med (1989) 170 (2): 499–509.
Citation
T Thepen, N Van Rooijen, G Kraal; Alveolar macrophage elimination in vivo is associated with an increase in pulmonary immune response in mice.. J Exp Med 1 August 1989; 170 (2): 499–509. doi: https://doi.org/10.1084/jem.170.2.499
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