IL-7/anti-IL-7 mAb complexes restore T cell development and induce homeostatic T Cell expansion without lymphopenia.

Détails

ID Serval
serval:BIB_DB7324141CDC
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
IL-7/anti-IL-7 mAb complexes restore T cell development and induce homeostatic T Cell expansion without lymphopenia.
Périodique
Journal of Immunology
Auteur(s)
Boyman O., Ramsey C., Kim D.M., Sprent J., Surh C.D.
ISSN
0022-1767
Statut éditorial
Publié
Date de publication
2008
Peer-reviewed
Oui
Volume
180
Numéro
11
Pages
7265-7275
Langue
anglais
Résumé
IL-7, a member of the common gamma-chain family of cytokines, is essential for B and T lymphocyte development and homeostasis of mature T cell subsets. Thus, naive and memory T cells are both dependent on IL-7 for survival and homeostatic proliferation under lymphopenic conditions. In line with prior findings with IL-2, we show in this study that the biological activity of IL-7 in vivo is greatly increased by association with anti-IL-7 mAb. Under in vivo conditions, IL-7/mAb complexes displayed 50- to 100-fold higher activity than free IL-7 and induced massive expansion of pre-B cells. IL-7/mAb complexes also increased thymopoiesis in normal mice and restored thymopoeisis in IL-7-deficient mice. For mature T cells, IL-7/mAb complexes induced marked homeostatic proliferation of both naive and memory CD4(+) and CD8(+) cell subsets even under normal T cell-replete conditions. Finally, IL-7/mAb complexes were able to enhance the magnitude of the primary response of Ag-specific naive CD8(+) cells. The strong stimulatory activity of IL-7/mAb complexes could be useful for treatment of immunodeficiency and cancer.
Mots-clé
Animals, Antigen-Antibody Complex, CD8-Positive T-Lymphocytes, Cell Proliferation, Homeostasis, Immunologic Memory, Interleukin-7, Lymphopenia, Mice, Mice, Inbred C57BL, Recombinant Proteins, T-Lymphocyte Subsets
Pubmed
Web of science
Création de la notice
23/03/2009 10:29
Dernière modification de la notice
20/08/2019 16:00
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