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cDCl prime and are licensed by CD4`+ T cells to induce anti-tumour immunity

机译：CDCL PRIME并由CD4` + T细胞许可以诱导抗肿瘤免疫力

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Conventional type 1 dendritic cells perform antigen processing and priming of CD4(+)and CD8(+)T cells against tumour antigens, orchestrating their cross-talk to effect anti-tumour immunity.Conventional type 1 dendritic cells (cDC1)(1)are thought to perform antigen cross-presentation, which is required to prime CD8(+)T cells(2,3), whereas cDC2 are specialized for priming CD4(+)T cells(4,5). CD4(+)T cells are also considered to help CD8(+)T cell responses through a variety of mechanisms(6-11), including a process whereby CD4(+)T cells 'license' cDC1 for CD8(+)T cell priming(12). However, this model has not been directly tested in vivo or in the setting of help-dependent tumour rejection. Here we generated anXcr1(Cre)mouse strain to evaluate the cellular interactions that mediate tumour rejection in a model requiring CD4(+)and CD8(+)T cells. As expected, tumour rejection required cDC1 and CD8(+)T cell priming required the expression of major histocompatibility class I molecules by cDC1. Unexpectedly, early priming of CD4(+)T cells against tumour-derived antigens also required cDC1, and this was not simply because they transport antigens to lymph nodes for processing by cDC2, as selective deletion of major histocompatibility class II molecules in cDC1 also prevented early CD4(+)T cell priming. Furthermore, deletion of either major histocompatibility class II or CD40 in cDC1 impaired tumour rejection, consistent with a role for cognate CD4(+)T cell interactions and CD40 signalling in cDC1 licensing. Finally, CD40 signalling in cDC1 was critical not only for CD8(+)T cell priming, but also for initial CD4(+)T cell activation. Thus, in the setting of tumour-derived antigens, cDC1 function as an autonomous platform capable of antigen processing and priming for both CD4(+)and CD8(+)T cells and of the direct orchestration of their cross-talk that is required for optimal anti-tumour immunity.
机译：常规1型树突细胞对肿瘤抗原进行CD4（+）和CD8（+）T细胞的抗原处理和引发，其串扰以实现抗肿瘤免疫。转化型1型树突细胞（CDC1）（1）是思想进行抗原交叉呈递，这是素序的CD8（+）T细胞（2,3），而CDC2专门用于引发CD4（+）T细胞（4,5）。还考虑CD4（+）T细胞来帮助CD8（+）T细胞通过各种机制（6-11）反应，包括用于CD8（+）T细胞CD4（+）T细胞的CDC1的方法灌注（12）。然而，该模型尚未在体内直接测试或在依赖依赖性肿瘤排斥的设置中进行测试。在这里，我们产生了ANXCR1（CRE）小鼠菌株，以评估介导需要CD4（+）和CD8（+）T细胞的模型中肿瘤排斥的细胞相互作用。正如预期的那样，肿瘤排斥所需的CDC1和CD8（+）T细胞引发需要通过CDC1表达主要组织相容性I分子。出乎意料地，CD4（+）T细胞对肿瘤衍生的抗原的早期引发也需要CDC1，这不仅仅是因为它们将抗原运输到淋巴结通过CDC2加工，因为选择性缺失CDC1中的主要组织相容性II类分子也被预防早期CD4（+）T细胞灌注。此外，在CDC1受损的肿瘤排斥中缺少主要组织相容性II或CD40，与CDC1许可中的CD4（+）T细胞相互作用和CD40信号传导的作用一致。最后，CDC1中的CD40信号传导不仅适用于CD8（+）T细胞引发，而且对于初始CD4（+）T细胞激活是至关重要的。因此，在肿瘤衍生的抗原的设置中，CDC1用作能够进行抗原处理和CD4（+）和CD8（+）T细胞的抗原加工和引发的自主平台，以及它们的串扰所需的直接编程最佳的抗肿瘤免疫力。

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  • 来源
    《Nature》 |2020年第7822期|624-629|共6页
  • 作者

    Ferris Stephen T.; Durai Vivek; Wu Renee; Theisen Derek J.; Ward Jeffrey P.; Bern Michael D.; Davidson Jesse T.; Bagadia Prachi; Liu Tiantian; Briseno Carlos G.; Li Lijin; Gillanders William E.; Wu Gregory F.; Yokoyama Wayne M.; Murphy Theresa L.; Schreiber Robert D.; Murphy Kenneth M.;

  • 作者单位

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA|Univ Calif San Francisco Dept Med San Francisco CA USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA|Washington Univ Sch Med Dept Med Div Oncol St Louis MO 63110 USA;

    Washington Univ Sch Med Div Rheumatol St Louis MO USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA|Washington Univ Sch Med Dept Surg St Louis MO 63110 USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA;

    Washington Univ Sch Med Dept Surg St Louis MO 63110 USA;

    Washington Univ Sch Med Dept Surg St Louis MO 63110 USA|Alvin J Siteman Canc Ctr Barnes Jewish Hosp St Louis MO USA|Washington Univ Sch Med St Louis MO USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA|Washington Univ Sch Med Dept Neurol St Louis MO 63110 USA;

    Washington Univ Sch Med Div Rheumatol St Louis MO USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA|Washington Univ Sch Med Andrew M & Jane M Bursky Ctr Human Immunol & Immu St Louis MO 63110 USA|Parker Inst Canc Immunotherapy San Francisco CA USA;

    Washington Univ Sch Med Dept Pathol & Immunol St Louis MO 63110 USA|Washington Univ Sch Med Howard Hughes Med Inst St Louis MO 63110 USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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