Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

C/EBPα Is Dispensable for the Ontogeny of PD-1+ CD4+ Memory T Cells but Restricts Their Expansion in an Age-Dependent Manner

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. Kinetics of the soluble urokinase plasminogen activator receptor (suPAR) in cirrhosis

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Incidence, prevalence and risk factors for hepatitis C in Danish prisons

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. Mutant CEBPA directly drives the expression of the targetable tumor-promoting factor CD73 in AML

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Heterozygous loss of Srp72 in mice is not associated with major hematological phenotypes

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. A programmed wave of uridylation-primed mRNA degradation is essential for meiotic progression and mammalian spermatogenesis

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. The splicing factor RBM25 controls MYC activity in acute myeloid leukemia

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  5. Leukemogenic nucleophosmin mutation disrupts the transcription factor hub regulating granulo-monocytic fates

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer
Ageing and cancer is often associated with altered T cell distributions and this phenomenon has been suggested to be the main driver in the development of immunosenescence. Memory phenotype PD-1+ CD4+ T cells accumulate with age and during leukemic development, and they might account for the attenuated T cell response in elderly or diseased individuals. The transcription factor C/EBPα has been suggested to be responsible for the accumulation as well as for the senescent features of these cells including impaired TCR signaling and decreased proliferation. Thus modulating the activity of C/EBPα could potentially target PD-1+ CD4+ T cells and consequently, impede the development of immunosenescence. To exploit this possibility we tested the importance of C/EBPα for the development of age-dependent PD-1+ CD4+ T cells as well as its role in the accumulation of PD-1+ CD4+ T cells during leukemic progression. In contrast to earlier suggestions, we find that loss of C/EBPα expression in the lymphoid compartment led to an increase of PD-1+ CD4+ T cells specifically in old mice, suggesting that C/EBPα repress the accumulation of these cells in elderly by inhibiting their proliferation. Furthermore, C/EBPα-deficiency in the lymphoid compartment had no effect on leukemic development and did not affect the accumulation of PD-1+ CD4+ T cells. Thus, in addition to contradict earlier suggestions of a role for C/EBPα in immunosenescence, these findings efficiently discard the potential of using C/EBPα as a target for the alleviation of ageing/cancer-associated immunosenescence.
OriginalsprogEngelsk
TidsskriftP L o S One
Vol/bind9
Udgave nummer1
Sider (fra-til)e84728
ISSN1932-6203
DOI
StatusUdgivet - 2014

ID: 42873291