Suppr超能文献

传染性单核细胞增多症样综合征中对CD40配体、CD4(+) T细胞和B细胞的需求

Requirement for CD40 ligand, CD4(+) T cells, and B cells in an infectious mononucleosis-like syndrome.

作者信息

Brooks J W, Hamilton-Easton A M, Christensen J P, Cardin R D, Hardy C L, Doherty P C

机构信息

Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.

出版信息

J Virol. 1999 Nov;73(11):9650-4. doi: 10.1128/JVI.73.11.9650-9654.1999.

Abstract

Respiratory challenge with the murine gammaherpesvirus 68 (gammaHV-68) results in productive infection of the lung, the establishment of latency in B lymphocytes and other cell types, transient splenomegaly, and prolonged clonal expansion of activated CD8(+) CD62L(lo) T cells, particularly a Vbeta4(+) CD8(+) population that is found in mice with different major histocompatibility complex (MHC) haplotypes. Aspects of the CD8(+)-T-cell response are substantially modified in mice that lack B cells, CD4(+) T cells, or the CD40 ligand (CD40L). The B-cell-deficient mice show no increase in Vbeta4(+) CD8(+) T cells. Similar abrogation of the Vbeta4(+) CD8(+) response is seen following antibody-mediated depletion of the CD4(+) subset, through the numbers of CD8(+) CD62L(lo) cells are still significantly elevated. Virus-specific CD4(+)-T-cell frequencies are minimal in the CD40L(-/-) mice, and the Vbeta4(+) CD8(+) population remains unexpanded. Apparently B-cell-CD4(+)-T-cell interactions play a part in the gammaHV-68 induction of both splenomegaly and non-MHC-restricted Vbeta4(+) CD8(+)-T-cell expansion.

摘要

用鼠γ疱疹病毒68(γHV - 68)进行呼吸道攻击会导致肺部产生感染、在B淋巴细胞和其他细胞类型中建立潜伏状态、出现短暂性脾肿大以及活化的CD8(+)CD62L(lo)T细胞的长期克隆性扩增,特别是在具有不同主要组织相容性复合体(MHC)单倍型的小鼠中发现的Vβ4(+)CD8(+)群体。在缺乏B细胞、CD4(+)T细胞或CD40配体(CD40L)的小鼠中,CD8(+)-T细胞反应的各个方面会发生显著改变。B细胞缺陷型小鼠的Vβ4(+)CD8(+)T细胞没有增加。在通过抗体介导耗尽CD4(+)亚群后,也会出现类似的Vβ4(+)CD8(+)反应的消除,不过CD8(+)CD62L(lo)细胞的数量仍然显著升高。在CD40L(-/-)小鼠中,病毒特异性CD4(+)-T细胞频率极低,并且Vβ4(+)CD8(+)群体仍未扩增。显然,B细胞与CD4(+)T细胞之间的相互作用在γHV - 68诱导脾肿大和非MHC限制性Vβ4(+)CD8(+)-T细胞扩增中发挥作用。

相似文献

1
Requirement for CD40 ligand, CD4(+) T cells, and B cells in an infectious mononucleosis-like syndrome.
J Virol. 1999 Nov;73(11):9650-4. doi: 10.1128/JVI.73.11.9650-9654.1999.
2
T cell reactivity during infectious mononucleosis and persistent gammaherpesvirus infection in mice.
J Immunol. 2004 Mar 1;172(5):3078-85. doi: 10.4049/jimmunol.172.5.3078.
4
Tuning into immunological dissonance: an experimental model for infectious mononucleosis.
Curr Opin Immunol. 1997 Aug;9(4):477-83. doi: 10.1016/s0952-7915(97)80098-2.
9
Changing patterns of dominance in the CD8+ T cell response during acute and persistent murine gamma-herpesvirus infection.
Eur J Immunol. 1999 Apr;29(4):1059-67. doi: 10.1002/(SICI)1521-4141(199904)29:04<1059::AID-IMMU1059>3.0.CO;2-L.

引用本文的文献

1
What do animal models tell us about the role of EBV in the pathogenesis of multiple sclerosis?
Front Immunol. 2022 Nov 17;13:1036155. doi: 10.3389/fimmu.2022.1036155. eCollection 2022.
2
Insights into CD8 T Cell Activation and Exhaustion from a Mouse Gammaherpesvirus Model.
Viral Immunol. 2020 Apr;33(3):215-224. doi: 10.1089/vim.2019.0183.
4
The murine gammaherpesvirus immediate-early Rta synergizes with IRF4, targeting expression of the viral M1 superantigen to plasma cells.
PLoS Pathog. 2014 Aug 7;10(8):e1004302. doi: 10.1371/journal.ppat.1004302. eCollection 2014 Aug.
5
BAFF receptor deficiency limits gammaherpesvirus infection.
J Virol. 2014 Apr;88(8):3965-75. doi: 10.1128/JVI.03497-13. Epub 2014 Feb 5.
6
Glycoprotein B cleavage is important for murid herpesvirus 4 to infect myeloid cells.
J Virol. 2013 Oct;87(19):10828-42. doi: 10.1128/JVI.00709-13. Epub 2013 Jul 31.
7
The absence of M1 leads to increased establishment of murine gammaherpesvirus 68 latency in IgD-negative B cells.
J Virol. 2013 Mar;87(6):3597-604. doi: 10.1128/JVI.01953-12. Epub 2013 Jan 9.
8
Ataxia telangiectasia mutated kinase controls chronic gammaherpesvirus infection.
J Virol. 2012 Dec;86(23):12826-37. doi: 10.1128/JVI.00917-12. Epub 2012 Sep 19.
9
Murine gammaherpesvirus 68 infection protects lupus-prone mice from the development of autoimmunity.
Proc Natl Acad Sci U S A. 2012 May 1;109(18):E1092-100. doi: 10.1073/pnas.1203019109. Epub 2012 Apr 2.
10

本文引用的文献

1
Changing patterns of dominance in the CD8+ T cell response during acute and persistent murine gamma-herpesvirus infection.
Eur J Immunol. 1999 Apr;29(4):1059-67. doi: 10.1002/(SICI)1521-4141(199904)29:04<1059::AID-IMMU1059>3.0.CO;2-L.
2
CD4(+) T cell-mediated control of a gamma-herpesvirus in B cell-deficient mice is mediated by IFN-gamma.
Proc Natl Acad Sci U S A. 1999 Apr 27;96(9):5135-40. doi: 10.1073/pnas.96.9.5135.
3
Quantitative analysis of the acute and long-term CD4(+) T-cell response to a persistent gammaherpesvirus.
J Virol. 1999 May;73(5):4279-83. doi: 10.1128/JVI.73.5.4279-4283.1999.
4
Macrophages are the major reservoir of latent murine gammaherpesvirus 68 in peritoneal cells.
J Virol. 1999 Apr;73(4):3273-83. doi: 10.1128/JVI.73.4.3273-3283.1999.
7
Virus-specific CD8(+) T cell numbers are maintained during gamma-herpesvirus reactivation in CD4-deficient mice.
Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15565-70. doi: 10.1073/pnas.95.26.15565.
9
The CD40-CD154 system in anti-infective host defense.
Curr Opin Immunol. 1997 Aug;9(4):491-7. doi: 10.1016/s0952-7915(97)80100-8.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验