Tosato G, Magrath I, Koski I, Dooley N, Blaese M
N Engl J Med. 1979 Nov 22;301(21):1133-7. doi: 10.1056/NEJM197911223012101.
Infectious mononucleosis is caused by the Epstein-Barr virus (EBV), an unusual human pathogen because it preferentially infects B lymphocytes and consequently activates them to produce immunoglobulins. When cultures of lymphocytes from patients with infectious mononucleosis were stimulated with polyclonal activators, unseparated cells failed to produce immunoglobulins, whereas purified B cells responded normally. Cocultures demonstrated profound suppressor T-cell activity in blood from patients with infectious mononucleosis. Early in this disease, circulating immunoglobulin-secreting cells were elevated, but during the second week their number was strikingly depressed. These data indicate that during infectious mononucleosis, EBV causes polyclonal activation of B cells, reflected by hypergammaglobulinemia and increased circulating immunoglobulin-secreting cells. Next, suppressor T cells become activated and inhibit further B-cell activation. Thus, activation of suppressor T cells in infectious mononucleosis provides a unique additional mechanism of host defense because these T cells inhibit the activation and proliferation of an important target of the causative virus.
传染性单核细胞增多症由爱泼斯坦-巴尔病毒(EBV)引起,EBV是一种特殊的人类病原体,因为它优先感染B淋巴细胞并使其活化以产生免疫球蛋白。当用多克隆激活剂刺激传染性单核细胞增多症患者的淋巴细胞培养物时,未分离的细胞无法产生免疫球蛋白,而纯化的B细胞反应正常。共培养显示传染性单核细胞增多症患者血液中存在显著的抑制性T细胞活性。在该病早期,循环中的免疫球蛋白分泌细胞增多,但在第二周其数量显著减少。这些数据表明,在传染性单核细胞增多症期间,EBV导致B细胞多克隆活化,表现为高球蛋白血症和循环免疫球蛋白分泌细胞增加。接下来,抑制性T细胞被激活并抑制B细胞的进一步活化。因此,传染性单核细胞增多症中抑制性T细胞的激活提供了一种独特的额外宿主防御机制,因为这些T细胞抑制致病病毒重要靶标的活化和增殖。