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Local macrophage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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Local macrophage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation. / Jenkins, Stephen J; Ruckerl, Dominik; Cook, Peter C et al.
In: Science, Vol. 332, No. 6035, 10.06.2011, p. 1284-1288.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Jenkins, SJ, Ruckerl, D, Cook, PC, Jones, LH, Finkelman, FD, van Rooijen, N, MacDonald, AS & Allen, JE 2011, 'Local macrophage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation', Science, vol. 332, no. 6035, pp. 1284-1288. https://doi.org/10.1126/science.1204351

APA

Jenkins, S. J., Ruckerl, D., Cook, P. C., Jones, L. H., Finkelman, F. D., van Rooijen, N., MacDonald, A. S., & Allen, J. E. (2011). Local macrophage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation. Science, 332(6035), 1284-1288. https://doi.org/10.1126/science.1204351

Vancouver

Jenkins SJ, Ruckerl D, Cook PC, Jones LH, Finkelman FD, van Rooijen N et al. Local macrophage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation. Science. 2011 Jun 10;332(6035):1284-1288. doi: 10.1126/science.1204351

Author

Jenkins, Stephen J ; Ruckerl, Dominik ; Cook, Peter C et al. / Local macrophage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation. In: Science. 2011 ; Vol. 332, No. 6035. pp. 1284-1288.

Bibtex

@article{c94a79cc8b534515acf7b6e1dd9e95bc,
title = "Local macrophage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation",
abstract = "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 (T(H)2)-related pathologies under the control of the archetypal T(H)2 cytokine interleukin-4 (IL-4) and was a fundamental component of T(H)2 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.",
keywords = "Animals, Blood, Brugia malayi, Cell Proliferation, Female, Filariasis, Filarioidea, Inflammation, Interleukin-4, Macrophage Activation, Macrophages, Male, Mice, Mice, Inbred C57BL, Monocytes, Th2 Cells, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S.",
author = "Jenkins, {Stephen J} and Dominik Ruckerl and Cook, {Peter C} and Jones, {Lucy H} and Finkelman, {Fred D} and {van Rooijen}, Nico and MacDonald, {Andrew S} and Allen, {Judith E}",
year = "2011",
month = jun,
day = "10",
doi = "10.1126/science.1204351",
language = "English",
volume = "332",
pages = "1284--1288",
journal = "Science",
issn = "0036-8075",
publisher = "American Association for the Advancement of Science",
number = "6035",

}

RIS

TY - JOUR

T1 - Local macrophage proliferation, rather than recruitment from the blood, is a signature of TH2 inflammation

AU - Jenkins, Stephen J

AU - Ruckerl, Dominik

AU - Cook, Peter C

AU - Jones, Lucy H

AU - Finkelman, Fred D

AU - van Rooijen, Nico

AU - MacDonald, Andrew S

AU - Allen, Judith E

PY - 2011/6/10

Y1 - 2011/6/10

N2 - 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 (T(H)2)-related pathologies under the control of the archetypal T(H)2 cytokine interleukin-4 (IL-4) and was a fundamental component of T(H)2 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.

AB - 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 (T(H)2)-related pathologies under the control of the archetypal T(H)2 cytokine interleukin-4 (IL-4) and was a fundamental component of T(H)2 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.

KW - Animals

KW - Blood

KW - Brugia malayi

KW - Cell Proliferation

KW - Female

KW - Filariasis

KW - Filarioidea

KW - Inflammation

KW - Interleukin-4

KW - Macrophage Activation

KW - Macrophages

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Monocytes

KW - Th2 Cells

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

KW - Research Support, U.S. Gov't, Non-P.H.S.

U2 - 10.1126/science.1204351

DO - 10.1126/science.1204351

M3 - Journal article

C2 - 21566158

VL - 332

SP - 1284

EP - 1288

JO - Science

JF - Science

SN - 0036-8075

IS - 6035

ER -