GM-CSF Controls Nonlymphoid Tissue Dendritic Cell Homeostasis but Is Dispensable for the Differentiation of Inflammatory Dendritic Cells

Melanie Greter, Julie Helft, Andrew Chow, Daigo Hashimoto, Arthur Mortha, Judith Agudo-Cantero, Milena Bogunovic, Emmanuel L. Gautier, Jennifer Miller, Marylene Leboeuf, Geming Lu, Costica Aloman, Brian D. Brown, Jeffrey W. Pollard, Huabao Xiong, Gwendalyn J. Randolph, Jerry E. Chipuk, Paul S. Frenette, Miriam Merad

Research output: Contribution to journalArticle

263 Scopus citations

Abstract

GM-CSF (Csf-2) is a critical cytokine for the in vitro generation of dendritic cells (DCs) and is thought to control the development of inflammatory DCs and resident CD103+ DCs in some tissues. Here we showed that in contrast to the current understanding, Csf-2 receptor acts in the steady state to promote the survival and homeostasis of nonlymphoid tissue-resident CD103+ and CD11b+ DCs. Absence of Csf-2 receptor on lung DCs abrogated the induction of CD8+ T cell immunity after immunization with particulate antigens. In contrast, Csf-2 receptor was dispensable for the differentiation and innate function of inflammatory DCs during acute injuries. Instead, inflammatory DCs required Csf-1 receptor for their development. Thus, Csf-2 is important in vaccine-induced CD8+ T cell immunity through the regulation of nonlymphoid tissue DC homeostasis rather than control of inflammatory DCs in vivo.

Original languageEnglish (US)
Pages (from-to)1031-1046
Number of pages16
JournalImmunity
Volume36
Issue number6
DOIs
StatePublished - Jun 29 2012

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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    Greter, M., Helft, J., Chow, A., Hashimoto, D., Mortha, A., Agudo-Cantero, J., Bogunovic, M., Gautier, E. L., Miller, J., Leboeuf, M., Lu, G., Aloman, C., Brown, B. D., Pollard, J. W., Xiong, H., Randolph, G. J., Chipuk, J. E., Frenette, P. S., & Merad, M. (2012). GM-CSF Controls Nonlymphoid Tissue Dendritic Cell Homeostasis but Is Dispensable for the Differentiation of Inflammatory Dendritic Cells. Immunity, 36(6), 1031-1046. https://doi.org/10.1016/j.immuni.2012.03.027