It is well-known that glial cells (including both astrocytes and microglia) play critical roles in the development of neuropathic pain [33–35]. Here, to further identify CD4+ T lymphocyte-mediated pathways, we also examined the lumbar spinal cord astrocytic response in CD4 KO mice via the analysis of GFAP expression. Our data suggest that the lack of CD4+ T lymphocytes is associated with a shorter-lasting L5Tx-induced increase of GFAP expression in the lumbar spinal cord. So far, no study has reported a potential interaction between infiltrating CD4+ T lymphocytes and astrocytes in the development of neuropathic pain. We suspect that Th1 CD4+ T lymphocytes could regulate astrocytes by both direct and indirect mechanisms. For instance, it is known that nitric oxide (NO) can induce GFAP expression [36] and that the Th1-related cytokines IFN-γ and TNF-α are known to be involved in NO production in the CNS [37]. Further, our previous observation of a reduction in the L5Tx-induced increase of microglia in the lumbar spinal cord in CD4 KO mice coupled with our GFAP results presented here suggest that CD4+ T lymphocytes may regulate astrocytic responses via microglia-mediated mechanisms [32]. Comprehensive in vitro and in vivo studies could be used to establish the interactions between Th1 CD4+ T lymphocytes and astrocytes in the future.