PMC:4136538 / 25376-26433 JSONTXT

{"project":"2_test","denotations":[{"id":"25143871-19923276-63946039","span":{"begin":37,"end":38},"obj":"19923276"},{"id":"25143871-19923276-63946039","span":{"begin":37,"end":38},"obj":"19923276"},{"id":"T76533","span":{"begin":37,"end":38},"obj":"19923276"},{"id":"T75311","span":{"begin":37,"end":38},"obj":"19923276"}],"text":"Unlike what was previously reported [8], we did not detect a significant increase in IFN-γ expression in the lumbar spinal cord post-L5Tx. This may be due to the different animal species used (rats vs. mice), the different assays used (polymerase chain reaction vs. ELISA), and/or the existence of multiple cellular sources of IFN-γ (including infiltrating T lymphocytes and macrophages and resident microglia and astrocytes). Nevertheless, we did detect significantly lower levels of IFN-γ in CD4 KO mice compared to WT mice at all times evaluated (including baseline), which could in part explain our previous observation that CD4 KO mice displayed significantly reduced hypersensitivity post-L5Tx. However, the cytokine mediators through which CD4+ T lymphocytes specifically promote the pathogenesis of the maintenance phase but not the initiation phase of neuropathic pain still need further investigation. We suspect that multiple cytokines are likely to be involved in this mechanism and that the cytokines are likely to work in a synergistic manner."}