Kurane I, Innis B L, Nimmannitya S, Nisalak A, Rothman A L, Livingston P G, Janus J, Ennis F A
Department of Medicine, University of Massachusetts Medical Center, Worcester 01655.
Southeast Asian J Trop Med Public Health. 1990 Dec;21(4):658-62.
Dengue fever (DF) and dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS) are major public health problems in many areas of the world. We are analyzing the human immune responses to dengue viruses, in order to understand the mechanism of recovery from dengue virus infections and the pathogenesis of DHF/DSS. Human natural killer (NK) cells lyse dengue virus-infected cells to a greater degree than uninfected cells. Antibodies to dengue viruses augment the lysis of dengue virus-infected cells by NK cells. Dengue virus-infected monocytes produce high levels of interferon alpha (IFN alpha). DR+ lymphocytes also produce high levels of IFN alpha after contact with dengue virus-infected monocytes. The IFN alpha produced protects uninfected monocytes from dengue virus infection. These results suggest that NK cells and IFN alpha may play an important role in controlling primary dengue virus infection. Dengue virus-specific CD4+CD8(-)T lymphocytes and CD4(-)CD8+T lymphocytes are present in the peripheral blood mononuclear cell population from donors who were infected with dengue virus. Most of CD4+T lymphocytes are dengue serotype-crossreactive. They lyse dengue virus-infected autologous cells in an HLA class II-restricted fashion, and produce interferon gamma (IFN gamma). IFN gamma augments dengue virus infection of monocytic cells in the presence of antidengue virus antibodies by increasing the number of Fc gamma receptors. Dengue virus-specific CD8+T lymphocytes lyse dengue virus-infected autologous cells in an HLA class I-restricted fashion. These CD8+T lymphocytes are also dengue serotype-crossreactive.(ABSTRACT TRUNCATED AT 250 WORDS)
登革热（DF）和登革出血热（DHF）/登革休克综合征（DSS）是世界许多地区的主要公共卫生问题。我们正在分析人类对登革病毒的免疫反应，以了解从登革病毒感染中恢复的机制以及DHF/DSS的发病机制。人类自然杀伤（NK）细胞对登革病毒感染细胞的裂解程度比对未感染细胞的裂解程度更高。登革病毒抗体可增强NK细胞对登革病毒感染细胞的裂解作用。登革病毒感染的单核细胞产生高水平的α干扰素（IFNα）。DR +淋巴细胞在与登革病毒感染的单核细胞接触后也会产生高水平的IFNα。产生的IFNα可保护未感染的单核细胞免受登革病毒感染。这些结果表明，NK细胞和IFNα可能在控制原发性登革病毒感染中起重要作用。登革病毒特异性CD4 + CD8（-）T淋巴细胞和CD4（-）CD8 + T淋巴细胞存在于感染登革病毒的供体的外周血单核细胞群体中。大多数CD4 + T淋巴细胞是登革热血清型交叉反应性的。它们以HLA II类限制性方式裂解登革病毒感染的自体细胞，并产生γ干扰素（IFNγ）。在存在抗登革病毒抗体的情况下，IFNγ通过增加Fcγ受体的数量来增强单核细胞对登革病毒的感染。登革病毒特异性CD8 + T淋巴细胞以HLA I类限制性方式裂解登革病毒感染的自体细胞。这些CD8 + T淋巴细胞也是登革热血清型交叉反应性的。（摘要截短为250字）
