RESUMO
<p><b>BACKGROUND</b>It is generally accepted that gliomas are the most common primary brain tumors with poor prognosis. We aimed to explore the relationship of the immunity of the central nervous system and the genesis and development of glioma.</p><p><b>METHODS</b>G422 glioma was implanted in the brain of BALB/c mice (immuno-competent mice), nude mice (T cell related immuno-deficient) and complement C3 knock-out mice (complement C3 related immunodeficient). The survival time of the host, growth and histopathology of the tumor, and concentrations of tumor necrosis factor-α (TNF-α) and interferon-γ (INF-γ) in tumor tissues were assessed.</p><p><b>RESULTS</b>Tumor spheres were formed in all mice after injection, and glial fibrillary acidic protein (GFAP) positive staining of the cells declared their glioma origin. The longest median survival time of (44.3 ± 6.0) days was found in BALB/c mice, followed by (24.8 ± 5.2) days in nude mice and the shortest (18.6 ± 5.8) days in complement C3 knock-out mice. Accordingly, the growth of the tumor was fastest in complement C3 knock-out mice, followed by the nude mice and slowest in the BALB/c mice. Although the proportions of infiltrating CD68(+) lymphocytes in tumor tissues showed no significant difference (P > 0.05), TNF-α level in the nude and C3 knock-out mice, (28.11 ± 4.86) µmol/L and (22.87 ± 6.36) µmol/L respectively, were significantly lower (P < 0.01) than that in the BALB/c mice, which was (230.21 ± 39.17) µmol/L. The INF-γ level was highest in the BALB/c mice ((180.76 ± 29.19) µmol/L), followed by the nude mice ((113.46 ± 23.76) µmol/L) and then the C3 knock-out mice ((16.84 ± 4.45) µmol/L).</p><p><b>CONCLUSIONS</b>The G422 glioma implanted in the brains of mice with different immune ability would be a useful model for studying the relationship of the immune system and tumor in the central nervous system. Furthermore, the T cells and complement C3 compartments of the immune response may affect the growth of implanted tumors and inflammatory factors such as TNF-α and INF-γ.</p>
