Induction of maturation of human blood dendritic cell precursors by measles virus is associated with immunosuppression.
Induction of maturation of human blood dendritic cell precursors by measles virus is associated with immunosuppression.
复制标题
麻疹病毒诱导人血液树突状细胞前体成熟与免疫抑制有关。
DOI:
--
复制
发表时间:
1997
影响因子:
11.1
通讯作者:
Schaulies
中科院分区:
文献类型:
--
作者:
Jens;J. Schnorr;S. Xanthakos;P. Keikavoussi;E. Kämpgen;V. Meulen;Sibylle Schneider;Schaulies
As well as inducing a protective immune response against reinfection, acute measles is associated with a marked suppression of immune functions against superinfecting agents and recall antigens, and this association is the major cause of the current high morbidity and mortality rate associated with measles virus (MV) infections. Dendritic cells (DCs) are antigen-presenting cells crucially involved in the initiation of primary and secondary immune responses, so we set out to define the interaction of MV with these cells. We found that both mature and precursor human DCs generated from peripheral blood monocytic cells express the major MV protein receptor CD46 and are highly susceptible to infection with both MV vaccine (ED) and wild-type (WTF) strains, albeit with different kinetics. Except for the down-regulation of CD46, the expression pattern of functionally important surface antigens on mature DCs was not markedly altered after MV infection. However, precursor DCs up-regulated HLA-DR, CD83, and CD86 within 24 h of WTF infection and 72 h after ED infection, indicating their functional maturation. In addition, interleukin 12 synthesis was markedly enhanced after both ED and WTF infection in DCs. On the other hand, MV-infected DCs strongly interfered with mitogen-dependent proliferation of freshly isolated peripheral blood lymphocytes in vitro. These data indicate that the differentiation of effector functions of DCs is not impaired but rather is stimulated by MV infection. Yet, mature, activated DCs expressing MV surface antigens do give a negative signal to inhibit lymphocyte proliferation and thus contribute to MV-induced immunosuppression.
DOI:
10.1073/pnas.93.6.2588
发表时间:
1996-03-19
影响因子:
11.1
作者:
Zhou, LJ;Tedder, TF
通讯作者:
Tedder, TF
影响因子:
3.7
作者:
Yanagi,Y;Cubitt,BA;Oldstone,MB
通讯作者:
Oldstone,MB
DOI:
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发表时间:
1988
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
作者:
McChesney,MB;Altman,A;Oldstone,MB
通讯作者:
Oldstone,MB