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  • Review Article
  • Published:

Monocyte differentiation and antigen-presenting functions

Key Points

  • Constitutively migrating LY6C+ monocytes can retain their own properties without differentiating into a bone fide macrophage or dendritic cell.

  • Monocytes can replenish tissue-specific macrophages if a residential macrophage niche opens.

  • Monocytes are as abundant as dendritic cell subsets in human and mouse lymph nodes in the steady state, and they are more abundant during inflammation.

  • Monocytes are antigen-presenting cells that load antigen on MHC class I and II molecules and prime CD8+ and CD4+ T cells.

  • Monocytes have both pro-inflammatory and anti-inflammatory properties.

  • Monocytes show plasticity and can differentiate into many different cell types in a manner that is dictated by the tissue environment.

Abstract

Monocytes develop in the bone marrow and represent the primary type of mononuclear phagocyte found in the blood. They were long thought of as a source for tissue macrophages, but recent studies indicate more complex roles for monocytes, both within the circulation and after their migration into tissues and lymphoid organs. In this Review, we discuss the newer concepts underlying the maturation of emigrating monocytes into different classes of tissue macrophages, as well as their potential functions, as monocyte-derived cells, in the tissues. In addition, we consider the emerging roles for monocytes in adaptive immunity as antigen-presenting cells.

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Figure 1: Monocyte recruitment under steady-state versus inflammatory conditions.
Figure 2: A comparison of monocytes and dendritic cells as antigen-presenting cells.

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Acknowledgements

The authors acknowledge support from the following National Institutes of Health grants: R01HL115334 (to C.V.J.), R37AI049653 (to G.J.R.) and R01HL114381 (to P.M.H.). They also thank T. D. Wager for carefully reading the manuscript.

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Jakubzick, C., Randolph, G. & Henson, P. Monocyte differentiation and antigen-presenting functions. Nat Rev Immunol 17, 349–362 (2017). https://doi.org/10.1038/nri.2017.28

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