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Abstract: The dorsal vagal complex (DVC) comprises three anatomically and functionally linked structures, the area postrema, the nucleus tractus solitarius, and the dorsal motor nucleus of the vagus nerve, forming a key hub for the integration of peripheral inflammatory information. These structures play a unique role at the neuroimmune interface, conveying peripheral immune signals to the brain and generating behavioral and physiological responses through two complementary pathways: a neural pathway, via vagal afferents projecting to the nucleus tractus solitarius, and a humoral pathway, via the area postrema, which lacks a blood–brain barrier and is therefore sensitive to circulating inflammatory mediators. Numerous studies have established that the DVC serves as a mandatory gateway for peripheral inflammatory signals, integrating this information prior to its transmission to forebrain centers and peripheral organs. Understanding this interface represents a major therapeutic challenge, as modulating the DVC and its circuits opens new avenues for the treatment of chronic inflammatory diseases and neurodegenerative disorders in which this interface is chronically disrupted. Paradoxically, despite this essential role in the regulation of inflammation, the phenotype of microglial cells, the resident immune cells of the central nervous system, has received very little attention in this region. In the present study, we characterized these cells by investigating the expression of Fc receptors for IgG and major histocompatibility complex class I and II. Our results reveal microglial subpopulations displaying an atypical phenotype in the healthy DVC, suggesting that these cells may serve as a specialized immunological interface capable of actively monitoring systemic signals.