Acquisition of HLA-DR and Costimulatory Molecules by T Cells from Allogeneic Antigen Presenting Cells

Game, David; Rogers, Nicola J.; Lechler, Robert I.

doi:10.1111/j.1600-6143.2005.00916.x

Cited by 78 publications

(80 citation statements)

References 42 publications

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“…These CD4 + T cells are type 1 helper T (Th) cells since they secrete IFN-γ, TNF-α and IL-2, but no IL-4. These CD4 + T cells carrying acquired APC Ag-presenting machinery can act as CD4 + Th1-APCs in stimulation of OVA-specific CD8 + CTL responses (22,81,83). In addition, CD4 + Th1-APCs also induce OVA-specific antitumor immunity in C57BL/6 mice against the OVAexpressing murine melanoma line BL6-10 OVA cells.…”

Section: Stimulatory Effect On Immune Responsesmentioning

confidence: 99%

“…CD4 + T cells that have captured agonist pMHC II complexes can subsequently present them to adjacent CD4 + T cells, and these T cells can proliferate in response to T cell-mediated presentation (83), but as the number of activated cells increases, this T-T cell interaction can result in apoptosis or the induction of anergy or tolerance or regulatory T cells (90)(91)(92). These mechanisms may serve to limit the clonol expansion (90).…”

Section: Suppressive Effect On Immune Responsesmentioning

confidence: 99%

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Intercellular Trogocytosis Plays an Important Role in Modulation of Immune Responses

et al. 2008

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Section: Stimulatory Effect On Immune Responsesmentioning

confidence: 99%

Section: Suppressive Effect On Immune Responsesmentioning

confidence: 99%

Intercellular Trogocytosis Plays an Important Role in Modulation of Immune Responses

et al. 2008

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“…Because CD86 is predominantly expressed on professional APCs (31), the presence of this protein on T cells might be a consequence of membrane transfer from CD86-expressing bystander cells (32,33) or the uptake of CD86-containing exosomes (34). Alternatively, the T cell phenotype might be affected by bystander cells through cell-cell interactions or secreted cytokines.…”

Section: Cd86 Expression On Cd4 + and Cd8 + T Cells Does Not Require mentioning

confidence: 99%

IL-2 Upregulates CD86 Expression on Human CD4+ and CD8+ T Cells

Paine

Kirchner²,

Immenschuh

et al. 2012

The Journal of Immunology

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The glycoprotein CD86 is an important costimulatory molecule that has been shown to be predominantly expressed on APCs, such as dendritic cells, macrophages, and B cells. More recently, CD86 was also detected on T cells in specific pathological conditions. The mechanisms of how CD86 might be induced and its functional role in T cells are not well understood. In the present study, we showed that treatment with IL-2 markedly upregulated CD86, but not CD80, in human CD4+ and CD8+ T cells. This upregulation occurred in the absence of bystander cells, and isolated naive CD4+ or CD8+ T cells exhibited different time-dependent CD86-expression patterns in response to IL-2. Upregulation of CD86 on activated T cells was reduced by Abs that block IL-2 and IL-2Rα (CD25), indicating a receptor-mediated mechanism. IL-2–dependent CD86 upregulation was blocked by pharmacological inhibitors of the NFAT and mammalian target of rapamycin pathways and was largely reduced by simultaneous exposure to IFN-α. Importantly, a marked increase in CD86 on T cells was also observed in vivo in IL-2–treated patients. In conclusion, IL-2 upregulates CD86 expression on human CD4+ and CD8+ T cells via a receptor-dependent mechanism that involves the NFAT and mammalian target of rapamycin pathways.

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“…Human T cells have also been described to acquire MHC and costimulatory molecules upon T cell-dendritic cell (DCs) interaction as well as adhesion molecules during transendothelial migration (8)(9)(10)(11). Human and murine T cells exchange molecules with DCs in a bidirectional manner (12).…”

mentioning

confidence: 99%

Antigen-Specific Transfer of Functional Programmed Death Ligand 1 from Human APCs onto CD8+ T Cells via Trogocytosis

Gary

Voelkl

Palmisano³

et al. 2012

The Journal of Immunology

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Upon specific interaction with APCs, T cells capture membrane fragments and surface molecules in a process termed trogocytosis. In this study, we demonstrate that human Ag-specific CD8+ T cells acquire the coinhibitory molecule programmed death ligand 1 (PD-L1) from mature dendritic cells (mDC) and tumor cells in an Ag-specific manner. Immature dendritic cells were less effective in transferring surface molecules onto CD8+ T cells than mDCs. Interestingly, trogocytosis of PD-L1 requires cell–cell contact and cannot be induced by uptake of soluble proteins obtained from mDC lysates. The transfer process is impaired by inhibition of vacuolar ATPases in T cells as well as by fixation of dendritic cells. Of importance, CD8+ T cells that acquired PD-L1 complexes were able to induce apoptosis of neighboring programmed death 1–expressing CD8+ T cells. In summary, our data demonstrate that human CD8+ T cells take up functionally active PD-L1 from APCs in an Ag-specific fashion, leading to fratricide of programmed death 1–expressing, neighboring T cells. The transfer of functionally active coinhibitory molecules from APCs onto human CD8+ T cells could have a regulatory role in immune responses.

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Acquisition of HLA-DR and Costimulatory Molecules by T Cells from Allogeneic Antigen Presenting Cells

Abstract: There is accumulating evidence that cell surface molecules may be transferred between cells during an encounter. The aim of these experiments was to determine whether transfer of allogeneic material to T cells could influence human alloresponses. CD4

Cited by 78 publications

References 42 publications

Intercellular Trogocytosis Plays an Important Role in Modulation of Immune Responses

Intercellular Trogocytosis Plays an Important Role in Modulation of Immune Responses

IL-2 Upregulates CD86 Expression on Human CD4+ and CD8+ T Cells

Antigen-Specific Transfer of Functional Programmed Death Ligand 1 from Human APCs onto CD8+ T Cells via Trogocytosis

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