Journal Article

DZNE-2026-00423

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png CD163 and Tim-4 identify resident intestinal macrophages that are spatially regulated by TGF-β.

Jayaraman, V. ; Prise, I. E. ; Kästele, V. ; Tamburrano, S. ; Wemyss, K. ; Bridgeman, H. M. ; Daw, R. H. ; Strangward, P. ; Sanderson, A. ; Cruickshank, S. M. ; Konkel, J. E. ; Chew, C. ; Yao, C. ; Anderson, C. J. ; Priller, J.DZNE* ; McColl, B. ; Munro, D. A. D. ; Martens, L. ; Scott, C. L. ; Guilliams, M. ; Adamson, A. D. ; Grainger, J. R. ; Shaw, T. N.

2026
Rockefeller Univ. Press New York, NY

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Please use a persistent id in citations: doi:10.1084/jem.20240801

Abstract: Macrophages localize in sub-tissular niches associated with their ontogeny and activity. In the intestine, a paradigm has emerged that long-lived macrophages are present in the muscular layer, while highly monocyte-replenished populations are found in the lamina propria (LP). Whether long-lived macrophages are restricted in such a simplified manner has not been well explored. Moreover, the impact of specific gut-associated factors on macrophage identity across intestinal tissue layers is unknown. We generated scRNA-seq data from WT and Ccr2-/- mice to identify phenotypic features of long-lived macrophage populations in distinct intestinal layers and identified CD163 as a marker to distinguish submucosal/muscularis (S/M) from LP macrophages. Challenging the emerging paradigm, long-lived macrophages were found in the LP and S/M, with distinct transcriptomes and responsiveness to proinflammatory stimuli. Employing transgenic mice, we demonstrate a critical role for TGF-β signalling in maintaining the identity of long-lived LP but not S/M macrophages and that macrophage-derived TGF-β1 is required to instruct intestinal macrophage identity after development.

Keyword(s): Animals (MeSH) ; Macrophages: metabolism (MeSH) ; CD163 Antigen (MeSH) ; Receptors, Cell Surface: metabolism (MeSH) ; Receptors, Cell Surface: genetics (MeSH) ; Antigens, Differentiation, Myelomonocytic: metabolism (MeSH) ; Antigens, Differentiation, Myelomonocytic: genetics (MeSH) ; Antigens, CD: metabolism (MeSH) ; Antigens, CD: genetics (MeSH) ; Mice (MeSH) ; Transforming Growth Factor beta: metabolism (MeSH) ; Intestinal Mucosa: metabolism (MeSH) ; Membrane Proteins: metabolism (MeSH) ; Membrane Proteins: genetics (MeSH) ; Mice, Knockout (MeSH) ; Receptors, CCR2: genetics (MeSH) ; Receptors, CCR2: metabolism (MeSH) ; Signal Transduction (MeSH) ; Intestines: cytology (MeSH) ; Transforming Growth Factor beta1: metabolism (MeSH) ; Mice, Inbred C57BL (MeSH) ; Mice, Transgenic (MeSH) ; CD163 Antigen ; Receptors, Cell Surface ; Antigens, Differentiation, Myelomonocytic ; Antigens, CD ; Transforming Growth Factor beta ; TIM-4 protein, mouse ; Membrane Proteins ; Receptors, CCR2 ; Transforming Growth Factor beta1

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Contributing Institute(s):

1. Translational Neuropsychiatry (AG Priller)

Research Program(s):

1. 353 - Clinical and Health Care Research (POF4-353) (POF4-353)

Appears in the scientific report 2026

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Database coverage:
; ; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Essential Science Indicators ; IF >= 15 ; JCR ; PubMed Central ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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