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Innervation of adipose tissue is essential for the proper function of this critical metabolic organ. Numerous surgical and chemical denervation studies have demonstrated how maintenance of brain-adipose communication through both sympathetic efferent and sensory afferent nerves helps regulate adipocyte size, cell number, lipolysis, and ‘browning’ of white adipose tissue. Neurotrophic factors are growth factors that promote neuron survival, regeneration and outgrowth of neurites from adult nerves. Peripheral blood immune cells have been shown to be a source of neurotrophic factors in humans and mice. Although a number of these immune cells also reside in the adipose stromal vascular fraction (SVF), it has remained unclear what roles they play in adipose innervation. We have demonstrated that adipose resident myeloid lineage immune cells secrete brain derived neurotrophic factor (BDNF) and that deletion of this neurotrophic factor from the myeloid lineage led to a ‘genetic denervation’ of inguinal subcutaneous adipose tissue, thereby causing decreased energy expenditure and increased adipose mass. AAV-BDNF intra-adipose injections resulted in an increase in markers of innervation in two models with demonstrated adipose neuropathy. We and others have previously shown that noradrenergic stimulation via cold exposure increases adipose innervation in the inguinal depot. Here we have identified a subset of myeloid cells that are Cx3cr1+ monocytes/macrophages expressing adrenergic receptors. The quantity of these mobile immune cells increased in adipose tissue upon cold stimulation, fitting with their function to hone to sites of tissue injury and repair, and these cells also expressed BDNF. We propose that these cold induced neuroimmune cells (CINCs) are key players in maintaining adipose innervation as well as promoting adipose nerve remodeling under adrenergic stimuli such as cold exposure. Graphical Abstract