Neuropathic pain is defined as pain caused by a lesion or disease of the somatosensory system. This debilitating illness affects roughly 7 percent of the population in the United States. Microglia, important immune cells in the central nervous system, are shown to play a critical role in the development of neuropathic pain. Peripheral nerve injury can activate spinal cord microglia to become pro-inflammatory versus anti-inflammatory phenotypes. CD137 ligand is a receptor on microglia that binds to the CD137 receptor on T lymphocytes. We have shown that CD137L knockout (KO) mice display reduced sensory sensitivity and faster functional recovery following sciatic nerve crush (SNC). We hypothesize that CD137L depletion induces this change through promoting microglia to preferentially differentiate into an anti-inflammatory subtype after SNC. Methods: To test this hypothesis, qRT-PCR and Flow Cytometry were used to measure the expression of markers specific to pro-vs anti-inflammatory microglia at various times following SNC in both wild-type (WT) and CD137L KO mice.