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Response to Comment on "Local CD11c⁺ MHC Class II^– Precursors Generate Lung Dendritic Cells during Respiratory Viral Infection, but Are Depleted in the Process"

Department of Respiratory Medicine, National Heart and Lung Institute, Imperial College London, London, United Kingdom

In our recent paper (1), we demonstrated that myeloid dendritic cells (DCs) can be generated in vitro in cultures supplemented with GM-CSF from lung CD11c⁺ MHC II^– cells. This observation led us to conclude that CD11c⁺ MHC II^– cells contain a population of DC precursors resident in naive lungs. We pointed out that the CD11c⁺ MHC II^– population is heterogeneous: 10% are CD11b⁺ cells (which may be DC precursors (2)), whereas others express F4/80 (probably identifying them as macrophage lineage). On light microscopy, isolated CD11c⁺ MHC II^– cells lack the vacuolization typical of macrophages and have a low cytoplasm/nucleus ratio. Morphologically, they have the appearance of activated lymphocytes rather than alveolar macrophages. Furthermore, macrophages are terminally differentiated cells and should not proliferate into DCs accordingly, whereas a subset of the cells we observed clearly proliferated. However, we agree that our data does not exclude the possibility that the CD11c⁺ MHC II^– population we have observed contained some alveolar or interstitial macrophages.

Furthermore, we observed a marked reduction in CD11c⁺ MHC II^– cells in the lung following respiratory syncytial viral infection parallel to the previously reported expansion of mature myeloid DCs. Numbers of CD11c⁺ MHC II^– cells remained low for weeks after infection, and we were unable to generate myeloid DCs from lung cells in vitro during that period. In addition, influenza infection does not induce a secondary expansion of myeloid lung DCs in mice previously infected with respiratory syncytial virus. Based on these findings, we suggest that the expansion and differentiation of DC precursors into mature myeloid DCs deplete these precursors from the lung for prolonged periods. To us, an exhaustion of DC precursor cells during their proliferation and differentiation into DCs does not seem paradoxical. If one assumes a prolonged lifespan of pulmonary myeloid DCs in situ, high numbers of these cells can be present despite very low numbers CD11c⁺ MHC II^– precursors.

References

1. Wang, H., N. Peters, V. Laza-Stanca, N. Nawroly, S. L. Johnston, J. Schwarze. 2006. Local CD11c⁺ MHC class II^– precursors generate lung dendritic cells during respiratory viral infection, but are depleted in the process. J. Immunol. 177: 2536-2542. [Abstract/Free Full Text]
2. von Garnier, C., L. Filgueira, M. Wikstrom, M. Smith, J. A. Thomas, D. H. Strickland, P. G. Holt, P. A. Stumbles. 2005. Anatomical location determines the distribution and function of dendritic cells and other APCs in the respiratory tract. J. Immunol. 175: 1609-1618. [Abstract/Free Full Text]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wang, H. Articles by Schwarze, J. Search for Related Content PubMed PubMed Citation Articles by Wang, H. Articles by Schwarze, J.