Local macrophage proliferation, rather than recruitment from the blood, is a signature of Th2 inflammation

By S. Jenkins, Dominik Ruckerl, P. Cook, L. Jones, F. Finkelman, N. Van Rooijen, A. MacDonald, J. Allen. Science, 2011

1,407 citations recorded by the source corpus.

Proliferation in situ, rather than immune cell recruitment, drives macrophage expansion in response to parasitic infection. A defining feature of inflammation is the accumulation of innate immune cells in the tissue that are thought to be recruited from the blood. We reveal that a distinct process exists in which tissue macrophages undergo rapid in situ proliferation in order to increase population density. This inflammatory mechanism occurred during T helper 2 (TH2)–related pathologies under the control of the archetypal TH2 cytokine interleukin-4 (IL-4) and was a fundamental component of TH2 inflammation because exogenous IL-4 was sufficient to drive accumulation of tissue macrophages through self-renewal. Thus, expansion of innate cells necessary for pathogen control or wound repair can occur without recruitment of potentially tissue-destructive inflammatory cells.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/23075a04761f3768eb43261e3d9fea90020993cf

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Citations in the corpus

INTERLEUKIN-4- AND INTERLEUKIN-13-MEDIATED ALTERNATIVELY ACTIVATED MACROPHAGES: ROLES IN HOMEOSTASIS AND DISEASE (2013, neutral): “The capacity for in situ self-renewal, however, does not appear to preclude overlaid contributions of blood-derived monocyte populations that assume the AAM phenotype during inflammatory responses, although monocyte subset characteristics in this regard appear to vary by experimental system (22, 25,”
Kupffer Cells in the Liver (2013, neutral): “macrophages, including Kupffer cells, can be stimulated to proliferate (55).”
Macrophage Phenotype and Function in Different Stages of Atherosclerosis (2016, neutral): “Moreover, IL-4 is a strong stimulus for macrophage proliferation.(14)”
Much More than M1 and M2 Macrophages, There are also CD169+ and TCR+ Macrophages (2015, background): “Nevertheless, IL-4-mediated proliferation seems to be independent of CSF-1 (25, 26).”
Embryonic and adult-derived resident cardiac macrophages are maintained through distinct mechanisms at steady state and during inflammation (2014, background): “In addition, it is also becoming apparent that tissue-resident macrophages are maintained and can expand dramatically by in situ proliferation, rather than recruitment of blood monocytes (Davies et al., 2013; Jenkins et al., 2011).”
From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation (2014, background): “Also, recruited monocytes can be directly polarized into an anti-inflammatory M2 phenotype by basophil-derived IL-4, in order to alleviate allergic inflammation in the skin (194).”
Macrophage heterogeneity in liver injury and fibrosis. (2014, background): “As such, the delivery of syngeneic mature macrophages, but not immature (precursor) monocytes, into CCl4treated mice reduced liver scarring by attracting other immune cells resulting in enhanced levels of the antifibrotic cytokine IL-10 and increased MMP-9 and -13 activation, accompanied by the elev”
Developmental and Functional Heterogeneity of Monocytes. (2018, background): “Nevertheless, in certain situations, such as helminth infections, IL-4 can drive the proliferation and the immune response of resident macrophages without the aid of recruited monocytes (Jenkins et al., 2011).”
Cancer-related inflammation: common themes and therapeutic opportunities. (2012, neutral): “nflammation [18].”