Cognate CD4+ T cell licensing of dendritic cells in CD8+ T cell immunity

@article{Smith2004CognateCT,
  title={Cognate CD4+ T cell licensing of dendritic cells in CD8+ T cell immunity},
  author={Christopher M. Smith and Nicholas S. Wilson and Jason C Waithman and Jose A. Villadangos and F. R. Carbone and William R. Heath and Gabrielle T. Belz},
  journal={Nature Immunology},
  year={2004},
  volume={5},
  pages={1143-1148}
}
Several studies have indicated that CD8+ T cells require CD4+ T cell help for memory formation. Evidence suggests that such help can be antigen independent, challenging whether the 'licensing' of dendritic cells (DCs) by CD4+ T cells is ever required for cytotoxic T lymphocyte (CTL) responses. We show here that help is essential for the generation of CTL immunity to herpes simplex virus 1 and that CD4+ T cells mediate help in a cognate, antigen-specific way. We provide direct in vivo evidence… 
cDC1 prime and are licensed by CD4 T cells to induce anti-tumour immunity
TLDR
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.
DENDRITIC CELLS REGULATE THE INDUCTION OF EFFECTOR AND MEMORY CD8+ T CELLS
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The role of DCs matured under conditions mimicking acute/early inflammation or mimicking chronic/late inflammation on the differentiation of CD8+ T cells is analyzed, widening the understanding of the mechanisms of DC-induced effector and memory cell differentiation and might lead to the improved DC-based cancer vaccines.
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TLDR
The role of iNKT cells is focused on in the cross-talk with cross-priming DC and memory CD8+ T cell formation, which enhances immune responses against bacterial pathogens or parasites but also play a role in viral infections.
CTL mobilization to virus-infected tissue requires CD4+ T cell help
TLDR
The results reveal a previously unappreciated role of CD4 help in mobilizing effector CTL to the peripheral sites of infection where they help to eliminate infected cells.
CD4+ T cells support cytotoxic T lymphocyte priming by controlling lymph node input
TLDR
The results reveal a previously unappreciated mode of CD4+ T-cell help, whereby they increase the input of naïve lymphocytes to the relevant LN for efficient screening of cognate CD8+ T cells.
Cutting Edge: Cognate CD4 Help Promotes Recruitment of Antigen-Specific CD8 T Cells around Dendritic Cells1
TLDR
The results support a model in which CD4 help operates rapidly, in part by favoring CD8 T cells recruitment around those DCs that are the most competent for priming.
The Roles of CD4+ T Cells in Tumor Immunity
TLDR
Recent advances in deciphering how anti-tumor immune responses are orchestrated by CD4+ T cells are reviewed, with a focus on the immunotherapeutic potential of CD 4+ T-cell manipulation in anti-Tumorimmune response.
Direct in vivo evidence of CD4+ T cell requirement for CTL response and memory via pMHC‐I targeting and CD40L signaling
TLDR
This study corroborates the coexistence of direct and indirect mechanisms of T cell help for a CTL response in noninflammatory situations and suggests a new “dynamic model of three‐cell interactions” for CTL immunity derived from stimulation by dissociated, licensed DCs, primed CD4+ T cells, and DC‐CD4- T cell clusters and may have significant implications for autoimmunity and vaccine design.
Requirement for CD70 in CD4+ Th Cell-Dependent and Innate Receptor-Mediated CD8+ T Cell Priming1
TLDR
It is demonstrated that CD70 is required for CD4+ T cell-dependent priming of CD8+ T cells as well as priming mediated by the viral signature, dsRNA, and it is suggested that expression of CD70 on DC represents the hallmark of conditioned DC.
T Cell Help Amplifies Innate Signals in CD8(+) DCs for Optimal CD8(+) T Cell Priming.
TLDR
T cell help is identified as a flexible means to amplify varying suboptimal innate signals in DCs and reversed the helper dependence of CD8(+) T cell priming upon HSV-1 skin infection.
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The results demonstrate that T-cell help is ‘programmed’ into CD8+ T cells during priming, conferring on these cells a hallmark of immune response memory: the capacity for functional expansion on re-encounter with antigen.
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It is shown that signalling through CD40 on the antigen-presenting cells can replace the requirement for TH cells, indicating that T-cell ‘help’, at least for generation of CTLs by cross-priming, is mediated by signalling throughCD40 onThe antigen- presenting cell.
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TLDR
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