Ma A, Datta M, Margosian E, Chen J, Horak I
Center for Blood Research, Harvard Medical School, Boston, Massachusetts 02115, USA.
J Exp Med. 1995 Nov 1;182(5):1567-72. doi: 10.1084/jem.182.5.1567.
Interleukin-2 (IL-2)-deficient (IL-2-/-) mice develop anemia and colonic inflammatory bowel disease. To elucidate the mechanism of this disease, we have bred IL-2-/- mice to two strains of immunodeficient mice, RAG-2-deficient (RAG-2-/-, lacking B and T cells) and JH-deficient mice (JH-/-, lacking B cells). IL-2-/-, RAG-2-/- double-mutant mice are disease free, while IL-2-/-, JH-/- double-mutant mice succumb to bowel disease at the same rate as IL-2-/- littermates. IL-2-/-, JH-/- mice do not, however, succumb to anemia. Thus, spontaneous intestinal inflammation in IL-2-/- mice requires mature T cells, not B cells, while anemia is dependent on B cells.
白细胞介素-2(IL-2)缺陷(IL-2-/-)小鼠会出现贫血和结肠炎性肠病。为阐明这种疾病的机制,我们将IL-2-/-小鼠与两种免疫缺陷小鼠品系进行杂交,即重组激活基因2缺陷(RAG-2-/-,缺乏B细胞和T细胞)小鼠和JH缺陷(JH-/-,缺乏B细胞)小鼠。IL-2-/-、RAG-2-/-双突变小鼠没有疾病,而IL-2-/-、JH-/-双突变小鼠患肠道疾病的几率与IL-2-/-同窝小鼠相同。然而,IL-2-/-、JH-/-小鼠不会患贫血。因此,IL-2-/-小鼠的自发性肠道炎症需要成熟的T细胞而非B细胞,而贫血则依赖于B细胞。