{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T06:06:51Z","timestamp":1784700411137,"version":"3.55.0"},"reference-count":65,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T00:00:00Z","timestamp":1784678400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    The capacity of fibroblasts to support macrophages predominantly through colony-stimulating factor 1 (CSF1)-mediated survival and proliferation has long been recognized. Whether macrophages actively regulate fibroblasts\n                    <jats:italic>in vivo<\/jats:italic>\n                    has remained a critical open question. Recent work in murine skin has provided the first direct evidence for reverse homeostatic licensing, a process whereby macrophages, in return, provide permissive signals that maintain fibroblast quiescence: conditional deletion of Csf1 in dermatopontin-expressing (Dpt+) fibroblasts causes a progressive loss of CD64+ and CD11c+ macrophages, which in turn deprives fibroblasts of essential microenvironmental cues, leading to disrupted cell-cycle, metabolic, and immune signaling programs, and compensatory fibroblast expansion. This discovery formally defines a bidirectional circuit. In human systemic sclerosis, elevated fibroblast-derived CSF1 and increased macrophage abundance jointly correlate with disease severity, a paradox we resolve through the concept of functional licensing exhaustion in disease-associated macrophages. Taking this breakthrough as a point of departure, we integrate the concept of a fibroblast-macrophage homeostatic circuit as a generalizable framework. We examine how this push-pull loop operates in tissue maintenance, wound repair, and fibrogenesis; explore its similarities and divergences in the tumor microenvironment and across organ fibroses; and propose a therapeutic shift from simple cell depletion to the restoration of circuit equilibrium. The framework provides a conceptual basis for clinical strategies that target stromal-immune interactions.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1917469","type":"journal-article","created":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T05:54:10Z","timestamp":1784699650000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["From support to homeostatic licensing: the bidirectional fibroblast\u2013macrophage circuit and its central role in tissue homeostasis and fibrosis"],"prefix":"10.3389","volume":"17","author":[{"given":"Meng","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Dermatology, Affiliated Hospital of Hebei University","place":["Baoding, Hebei, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruiqi","family":"Chu","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Affiliated Hospital of Hebei University","place":["Baoding, Hebei, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shengni","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Affiliated Hospital of Hebei University","place":["Baoding, Hebei, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiangxiang","family":"Ren","sequence":"additional","affiliation":[{"name":"Department of General Surgery, Affiliated Hospital of Hebei University","place":["Baoding, Hebei, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,22]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/s41590-026-02434-5","article-title":"Reciprocal regulation of fibroblast-macrophage equilibrium governs skin integrity","volume":"27","author":"Vollmers","year":"2026","journal-title":"Nat 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