![]() Proper organ development and homeostasis is reliant not only on the appropriate function of specialized tissue-specific stromal cells but also on the cross talk that occurs between these cells and the stably or transiently integrated tissue-resident immune cell populations. This AT2-AM relationship begins during embryogenesis, where nascent AT2s timely induce GM-CSF expression to support the proliferation and differentiation of fetal monocytes contemporaneously seeding the tissue, and persists into adulthood, when epithelial GM-CSF remains restricted to AT2s. Instead, AT2 lineage-specific constitutive and inducible Csf2 deletion revealed the nonredundant function of AT2-derived GM-CSF in instructing AM fate, establishing the postnatal AM compartment, and maintaining AMs in adult lungs. ![]() AMs were unaffected by constitutive deletion of hematopoietic Csf2 and basophil depletion. We thus developed new transgenic mice to profile pulmonary GM-CSF expression, which we detected in both immune cells, including group 2 innate lymphoid cells and γδ T cells, as well as AT2s. However, evidence to functionally link components of this intercellular cross talk remains scarce. For alveolar macrophages (AMs), these signals are provided by immune and nonimmune cells and include GM-CSF (CSF2). Programs defining tissue-resident macrophage identity depend on local environmental cues.
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