The involvement of adaptive immunity, particularly spinal cord-infiltrating CD4+ T lymphocytes, in the development of nerve injury-induced behavioral hypersensitivity has been well-accepted [3,4]. Several pre-clinical studies have provided evidence, such as the passive transfer of individual T lymphocyte subtypes and the measurement of tissue levels of Th1 cell-producing cytokines [6,8], that suggests that the Th1 subtype of CD4+ T lymphocytes plays a role in peripheral nerve injury-induced sensory hypersensitivity. However, there has been no direct examination of peripheral nerve injury-induced infiltrating CD4+ T lymphocytes. In the current study, we analyzed L5Tx-induced lumbar spinal cord-infiltrating CD4+ T lymphocytes by intracellular flow cytometric analysis via an array of Th1 and Th2 CD4+ T lymphocyte cellular markers. Our results directly show an increase in Th1, but not Th2, CD4+ T lymphocytes in the lumbar spinal cord following L5Tx and suggest that Th1 CD4+ T lymphocytes mediate their pronociceptive effects via multiple cytokines (such as IFN-γ, TNF-α, and GM-CSF). Interestingly, although all of the Th1 cytokines measured have been associated with nerve injury-induced pain behaviors [8,23–25], some of them have also been associated with nerve regeneration and the recovery of nerve function following nerve injury [24–26]. Further investigation of such cytokine-mediated effects will help elucidate the specific role of infiltrating CD4+ T lymphocytes in the development of neuropathic pain, and such knowledge could help in the design of therapies that would target the cytokines/mechanisms responsible for the maintenance of neuropathic pain while avoiding eliminating factors that have neuroprotective effects.