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Nat Commun. 2018 Oct 26;9(1):4483. doi: 10.1038/s41467-018-06804-y.

IL-7 receptor blockade blunts antigen-specific memory T cell responses and chronic inflammation in primates.

Author information

1
Centre de Recherche en Transplantation et Immunologie (CRTI) UMR1064, INSERM, Université de Nantes, Nantes, 44093, France.
2
OSE Immunotherapeutics, Nantes, 44200, France.
3
Quality Assistance, Thuin, 6536, Belgium.
4
ARNA laboratory, Université de Bordeaux, INSERM U1212, CNRS UMR5320, IECB, Bordeaux, 33076, France.
5
Institut de Transplantation Urologie Néphrologie (ITUN), CHU Nantes, Nantes, 44093, France.
6
Centre de Recherche en Transplantation et Immunologie (CRTI) UMR1064, INSERM, Université de Nantes, Nantes, 44093, France. nicolas.poirier@ose-immuno.com.
7
OSE Immunotherapeutics, Nantes, 44200, France. nicolas.poirier@ose-immuno.com.

Abstract

Targeting the expansion of pathogenic memory immune cells is a promising therapeutic strategy to prevent chronic autoimmune attacks. Here we investigate the therapeutic efficacy and mechanism of new anti-human IL-7Rα monoclonal antibodies (mAb) in non-human primates and show that, depending on the target epitope, a single injection of antagonistic anti-IL-7Rα mAbs induces a long-term control of skin inflammation despite repeated antigen challenges in presensitized monkeys. No modification in T cell numbers, phenotype, function or metabolism is observed in the peripheral blood or in response to polyclonal stimulation ex vivo. However, long-term in vivo hyporesponsiveness is associated with a significant decrease in the frequency of antigen-specific T cells producing IFN-γ upon antigen restimulation ex vivo. These findings indicate that chronic antigen-specific memory T cell responses can be controlled by anti-IL-7Rα mAbs, promoting and maintaining remission in T-cell mediated chronic inflammatory diseases.

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