Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Nat Immunol. 2012 Sep;13(9):843-50. doi: 10.1038/ni.2388. Epub 2012 Aug 5.

TGF-β is responsible for NK cell immaturity during ontogeny and increased susceptibility to infection during mouse infancy.

Author information

  • 1Department of Microbiology and Immunology, University of Michigan School of Medicine, Ann Arbor, Michigan, USA.

Erratum in

  • Nat Immunol. 2013 Aug;14(8):876.

Abstract

A large gap in our understanding of infant immunity is why natural killer (NK) cell responses are deficient, which makes infants more prone to viral infection. Here we demonstrate that transforming growth factor-β (TGF-β) was responsible for NK cell immaturity during infancy. We found more fully mature NK cells in CD11c(dnR) mice, whose NK cells lack TGF-β receptor (TGF-βR) signaling. Ontogenic maturation of NK cells progressed faster in the absence of TGF-β signaling, which results in the formation of a mature NK cell pool early in life. As a consequence, infant CD11c(dnR) mice efficiently controlled viral infections. These data thus demonstrate an unprecedented role for TGF-β in ontogeny that can explain why NK cell responses are deficient early in life.

PMID:
22863752
[PubMed - indexed for MEDLINE]
PMCID:
PMC3426626
Free PMC Article

Images from this publication.See all images (7)Free text

Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Nature Publishing Group Icon for PubMed Central
    Loading ...
    Write to the Help Desk