Depletion of CD25+ regulatory cells uncovers immune responses to shared murine tumor rejection antigens

Golgher, Denise; Jones, Emma; Powrie, Fiona; Elliott, Tim; Gallimore, Awen

doi:10.1002/1521-4141(200211)32:11<3267::aid-immu3267>3.0.co;2-1

Cited by 242 publications

(178 citation statements)

References 43 publications

(46 reference statements)

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“…Treatment with the mAb PC61 efficiently depletes CD25 + T cells as reported [38,39]. Depletion of CD25 + T cells from the graft of DP T cells (by either antibody treatment or electronic sorting of CD25 -DP T cells) revealed their colitogenic potential.…”

Section: Cd25 + T R Cells Attenuate the Colitis Induced By Mhc Class supporting

confidence: 56%

MHC class II‐independent CD25⁺ CD4⁺ CD8α β⁺ α β T cells attenuate CD4⁺ T cell‐induced transfer colitis

2004

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CD4 + § g T cell populations that develop in mice deficient in MHC class II (through 'knockout' of either the A § , or the A g chain of the I-A b molecule) comprise a major 'single-positive' (SP) CD4 + CD8 -subset (60-90%) and a minor 'double-positive' (DP) CD4 + CD8 § g + subset (10-40%). Many DP T cells found in spleen, mesenteric lymph nodes (MLN) and colonic lamina propria (cLP) express CD25, CD103 and Foxp3. Adoptive transfer of SP but not DP T cells from A § -/-or A g -/-B6 mice into congenic RAG -/-hosts induces colitis. Transfer of SP T cells repopulates the host with only SP T cells; transfer of DP T cells repopulates the host with DP and SP T cells. Anti-CD25 antibody treatment of mice transplanted with DP T cells induces severe, lethal colitis; anti-CD25 antibody treatment of mice transplanted with SP T cells further aggravates the course of severe colitis. Hence, regulatory CD25 + T cells within (or developing from) the DP T cell population of MHC class II-deficient mice control the colitogenic potential of CD25 -CD4 + T cells.

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Section: Cd25 + T R Cells Attenuate the Colitis Induced By Mhc Class supporting

confidence: 56%

MHC class II‐independent CD25⁺ CD4⁺ CD8α β⁺ α β T cells attenuate CD4⁺ T cell‐induced transfer colitis

2004

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“…Therapeutic targeting of Tregs has been used for murine and human cancer immunotherapy (27)(28)(29)(30)(31)(32)(33). Depletion of Tregs by administration of CTLA-4-specific Ab or CD25-specific Ab enhances the efficacy of tumor immunotherapy and mediates tumor regression (27)(28)(29)(30)(31)(32)(33).…”

Section: Discussionmentioning

confidence: 99%

The Indispensable Role of CCR5 for In Vivo Suppressor Function of Tumor-Derived CD103+ Effector/Memory Regulatory T Cells

Chang

Lin

Kang

et al. 2012

The Journal of Immunology

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CD103 is a marker for identification of effector/memory regulatory T cells (Tregs). CD103+ Tregs are potent suppressors of tissue inflammation in several infectious diseases, autoimmune diseases, and cancers. However, the underlying mechanisms for this potent suppression ability remain unclear. The current study was designed to clarify this issue. Unexpectedly, we found both CD103+ and CD103− Tregs had similar suppression capacity in vitro. We then chose a murine tumor model for investigation of the in vivo behavior of these Tregs. The suppression ability in vivo against the anti-tumor ability of CD8+ T cells was restricted to CD103+ Tregs although both Tregs had equal in vitro suppression ability. In addition, CD103+ Tregs expressed significantly higher levels of CCR5 than those of CD103− Tregs and accumulated more in tumors than did CD103− Tregs. Furthermore, blockade of CCR5 signaling, either by CCR5−/−CD103+ Tregs or by CCL5 knockdown tumor, could reduce the migration of CD103+ Tregs into tumors and impair their in vivo suppression ability. In conclusion, these results indicate that the potent in vivo suppression ability of CD103+ Tregs is due to the tissue-migration ability through CCR5 expression.

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“…However, if this was the case it might have been anticipated that the secondary response to antigen would have been diminished, and it is perhaps surprising that in these animals it was robust. Many groups have shown that depleting anti-CD25 mAb, such as PC61, can enhance the generation of functional effector T cells [20,[35][36][37]. We can only surmise that the outcome of anti-CD25 mAb therapy is model dependent and that the timing of administration of anti-CD25 mAb relative to immunisation with antigen is critical.…”

Section: Discussionmentioning

confidence: 99%

Optimising anti‐tumour CD8 T‐cell responses using combinations of immunomodulatory antibodies

et al. 2008

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Immunostimulatory mAb as vaccine adjuvants for the treatment of cancer hold considerable potential for boosting weak responses when used against immunogenic tumours, or in combination with various other vaccines. We now show that when administered with OVA, the combination of anti-4-1BB mAb with anti-CD40, anti-OX40 or anti-CD25 resulted in a fourfold enhancement in the antigen-specific T-cell response compared with anti-4-1BB mAb alone, with a similar enhancement in memory responses following rechallenge with OVA. Although the number of antigen-specific T-cells generated after treatment with each of the combinations was similar, marked functional differences were detected. In particular, anti-4-1BB/anti-CD25 resulted in excellent expansion of specific CD81 T cells but produced fewer IFN-c-secreting effector cells than the other combinations. Anti-4-1BB/anti-OX40 proved to be the most potent, inducing the most effective T-cell responses in the RIPmOVA diabetes model with adoptively transferred OVA-specific T cells, and, when given with a peptide vaccine, protecting mice against the poorly immunogenic B16-F10 tumour. Overall the results suggest that although these combinations of mAb look promising in terms of their therapeutic potential, further functional assays are needed to compare their effects.

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Depletion of CD25+ regulatory cells uncovers immune responses to shared murine tumor rejection antigens

Cited by 242 publications

References 43 publications

MHC class II‐independent CD25⁺ CD4⁺ CD8α β⁺ α β T cells attenuate CD4⁺ T cell‐induced transfer colitis

MHC class II‐independent CD25⁺ CD4⁺ CD8α β⁺ α β T cells attenuate CD4⁺ T cell‐induced transfer colitis

The Indispensable Role of CCR5 for In Vivo Suppressor Function of Tumor-Derived CD103+ Effector/Memory Regulatory T Cells

Optimising anti‐tumour CD8 T‐cell responses using combinations of immunomodulatory antibodies

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Depletion of CD25+ regulatory cells uncovers immune responses to shared murine tumor rejection antigens

Cited by 242 publications

References 43 publications

MHC class II‐independent CD25+ CD4+ CD8α β+ α β T cells attenuate CD4+ T cell‐induced transfer colitis

MHC class II‐independent CD25+ CD4+ CD8α β+ α β T cells attenuate CD4+ T cell‐induced transfer colitis

The Indispensable Role of CCR5 for In Vivo Suppressor Function of Tumor-Derived CD103+ Effector/Memory Regulatory T Cells

Optimising anti‐tumour CD8 T‐cell responses using combinations of immunomodulatory antibodies

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MHC class II‐independent CD25⁺ CD4⁺ CD8α β⁺ α β T cells attenuate CD4⁺ T cell‐induced transfer colitis

MHC class II‐independent CD25⁺ CD4⁺ CD8α β⁺ α β T cells attenuate CD4⁺ T cell‐induced transfer colitis