RESUMEN
OBJECTIVES: Myeloid-derived suppressor cells contribute to the immunosuppressive microenvironment during tumor development and limit the efficacy of cancer immunotherapy. Identifying myeloid-derived suppressor cells and associated factors is the first step in creating strategies to reverse the suppressive effects of these cells on the immune system. METHODS: To induce lung cancer, we administered 2 doses of urethane to BALB/c mice and observed these animals for 120 days. After this period, we evaluated the percentage of myeloid-derived suppressor cells in the blood, lung and bone marrow. The expression of alpha-smooth muscle actin, transforming growth factor-β, Toll-like receptor 2, Toll-like receptor 4, and interleukin-6 was also determined in the lung tissue. RESULTS: Myeloid-derived suppressor cells were increased in all evaluated tissues after lung cancer development in association with increased Toll-like receptor 4 expression and decreased interleukin-6 expression in the lung. We observed alpha-smooth muscle actin and transforming growth factor-β expression in lung nodules. CONCLUSIONS: We believe that the early diagnosis of cancer through determining the blood levels of myeloid-derived suppressor cells followed by the depletion of these cells should be further investigated as a possible approach for cancer treatment. .
Asunto(s)
Animales , Masculino , Ratones , Neoplasias Pulmonares/patología , Células Mieloides/patología , Actinas/metabolismo , Western Blotting , Carcinógenos , Citometría de Flujo , Inmunohistoquímica , /metabolismo , Neoplasias Pulmonares/inducido químicamente , Neoplasias Pulmonares/inmunología , Pulmón/efectos de los fármacos , Pulmón/patología , Ratones Endogámicos BALB C , Células Mieloides/inmunología , Factores de Tiempo , /metabolismo , UretanoRESUMEN
This report documents a case of myeloid erythrophagocytosis in a patient with myeloproliferative disorder. The patient had pancytopenia and his marrow was hyperplastic with erythrophagocytosis by myeloid cells of various stages, including myeloblasts. He was diagnosed to have a prefibrotic stage of chronic idiopathic myelofibrosis. The erythrophagocytosis by myeloid cells persisted even after 2 months of treatment for the primary disorder.