The homeostatic balance between production and elimination of CD4+ T cells in peripheral blood plays an important role in patients with neuromyelitis optica (NMO). The objective of the present study was to evaluate the anti-apoptosis genes Bcl-2 and its promoter signal (nuclear factor kappa-light-chain-enhancer of activated B cells, NF kappa B) in CD4+ T cells. Healthy subjects (HS, n = 25) and patients with multiple sclerosis (MS) (n = 25) and NMO (n = 30) in remission were consecutively enrolled in this prospective study between May and December 2015. CD4+ T cells were isolated using magnetic beads coated with anti-CD4 monoclonal antibodies, and gene expression of Bcl-2, NF kappa B, phosphatidylinositol-4, 5-bisphosphate 3-kinase/protein kinase B (PI3K/Akt), and MAP kinase kinase kinase 7 (MAP3K7) was measured by real-time reverse transcription-polymerase chain reaction (rt-PCR). Cytokines of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta were detected using human cytokine multiplex assay. Bcl-2 and NF kappa B gene expressions were elevated in NMO patients (1.63 +/- 0.25; 2.35 +/- 0.25) compared with those of HS (0.90 +/- 0.11; 1.42 +/- 0.22) and/or MS patients (1.03 +/- 0.18; 1.55 +/- 0.20) (P < 0.05). MAP3K7, but not Akt, was increased in NMO patients (1.23 +/- 0.18; 1.56 +/- 0.22) (P < 0.01) and was a significant factor related to elevated NF kappa B gene expressions (P < 0.001). On the other hand, IL-1 beta and TNF-alpha were also detected in the study and the results showed that both were elevated in NMO patients (23.84 +/- 1.81; 56.40 +/- 2.45) (P < 0.01; P < 0.05, respectively). We propose that MAP3K7 induced by IL-1 beta and TNF-alpha but not Akt promotes NF kappa B expression and, in turn, prolongs Bcl-2-mediated survival of CD4+ T cells in NMO patients.