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γδ T cells are a specialized type of T cells, which undergo an effector function pre-programming in the thymus, allowing them to respond rapidly to any stimuli in the periphery. These cells can be divided in IFN-γ producing γδ T cells and IL-17-producing γδ (γδ17) T cells. Among these, the γδ17 T cells are known for their variety of unconventional functions in the physiology of tissues such as the adipose tissue, reproductive system, gingiva, and bone. In recent work, the host laboratory discovered that the production of IL-17 by a meningeal population of Vγ6+ γδ T cells was crucial for hippocampal synaptic plasticity and short-term memory at steady state. This population was found to be the main source of IL-17 in the steady state central nervous system. On the other hand, the laboratory demonstrated that increased levels of meningeal IL-17 (mostly produced by γδ T cells) promoted the early onset of cognitive decline in a transgenic mouse model of Alzheimer’s disease. Therefore, we propose a dual role for meningeal IL-17, pro-cognitive at steady state and anti-cognitive in neurodegeneration. As the central nervous system IL-17 is mainly provided by meningeal γδ T cells, a tight regulation of this cell subset is essential to control the levels of IL-17 and thus, brain cognition. This dual role of IL-17 could be further expanded to other non-lymphoid tissues, where γδ T cells are also a major source of IL-17, becoming important to understand the factors that control the homeostasis of this cell subset with ramifications for global body homeostasis. Stress is a known modulator of the immune system. Accordingly, the host laboratory has characterized the transcriptome of γδ17 T cells from peripheral lymph nodes and found that these cells presented increased gene expression of Nr3c1 and Adrb2, encoding for receptors for stress-mediators glucocorticoids and catecholamines, in comparison with the other γδ T cell subsets. Consequently, we aim to study the role of catecholamines and glucocorticoids in the regulation of the homeostasis of Vγ6+ γδ17 T cells. We addressed our hypothesis by evaluating the impact of stress on γδ17 T cell homeostasis. For this, we subjected mice to a prolonged restraint stress protocol. We observed both a decreased proportion of γδ17 T cells and decreased production of IL-17 from this subset within the non-lymphoid tissues: meninges, adipose tissue, and testis. This decrease was specific to γδ17 T cells, as γδIFN T cells and IFN-γ production were unaltered. Furthermore, we dissected the molecular mechanisms responsible for this contraction through a series of in vivo and ex vivo approaches. We observed that the contraction of γδ17 T cells in non-lymphoid tissues was mainly mediated by glucocorticoids and that catecholamines were involved in an indirect mechanism of suppression of γδ17 T cells of the adipose tissue. To our knowledge, we are the first group to describe the contraction of γδ17 T cells in non-lymphoid tissues upon prolonged restraint stress. This work highlighted one of the multiple factors that control the homeostasis of γδ T cells. Further exploration of this project might undercover what are the key implications of stress in the distinct tissues homed by γδ17 T cells, with potential application for stress therapeutic strategies.