Social touch can act as a stress buffer, reducing behavioral and physiological responses to stressful scenarios. However, the skin-brain mechanosensory pathways that promote stress resilience remain unknown. In this thesis, I investigated how Mrgprb4-lineage touch neurons in the skin of mice play a role in this soothing skin-brain circuit. Early life ablation and activation of Mrgprb4-lineage neurons did not impact pup ultrasonic vocalizations, a measurement of postnatal stress. However, I found that mice with an early life genetic ablation of Mrgprb4-lineage touch neurons display behaviors that suggest vulnerability to stress in adulthood. Chemogenetic activation of the Mrgprb4-lineage touch neurons with whole brain activity mapping with c-Fos, uncovered distinct activity patterns in brain areas relevant to somatosensation, reward, and affect. Optogenetic activation of these neurons also promoted a conditioned place preference in female mice. Lasty, attempting to rescue deficits brought on by stress, we chemogenetically activated Mrgprb4-lineage neurons in adulthood and observed a reduction in corticosterone under mild acute stress conditions. Together, these studies reveal that Mrgprb4-lineage sensory neurons in the skin engage networks across the brain as part of a skin-brain pathway for stress resilience in mice.