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Hrdinka M, Sudan K, Just S, et al. Normal Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice. PLoS One. 2016;11(9):e0162863doi: 10.1371/journal.pone.0162863.
Hrdinka, M., Sudan, K., Just, S., Drobek, A., Stepanek, O., Schlüter, D., Reinhold, D., Jordan, B. A., Gintschel, P., Schraven, B., & Kreutz, M. R. (2016). Normal Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice. PloS one, 11(9), e0162863. https://doi.org/10.1371/journal.pone.0162863
Hrdinka, Matous, et al. "Normal Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice." PloS one vol. 11,9 (2016): e0162863. doi: https://doi.org/10.1371/journal.pone.0162863
Hrdinka M, Sudan K, Just S, Drobek A, Stepanek O, Schlüter D, Reinhold D, Jordan BA, Gintschel P, Schraven B, Kreutz MR. Normal Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice. PLoS One. 2016 Sep 22;11(9):e0162863. doi: 10.1371/journal.pone.0162863. eCollection 2016. PMID: 27657535; PMCID: PMC5033326.
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PLoS One. 2016 Sep 22;11(9):e0162863. doi: 10.1371/journal.pone.0162863. eCollection 2016.

Normal Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice.

PloS one

Matous Hrdinka, Kritika Sudan, Sissy Just, Ales Drobek, Ondrej Stepanek, Dirk Schlüter, Dirk Reinhold, Bryen A Jordan, Patricia Gintschel, Burkhart Schraven, Michael R Kreutz

Affiliations

  1. RG Neuroplasticity, Leibniz-Institute for Neurobiology, Magdeburg, Germany.
  2. Institute of Molecular and Clinical Immunology, Otto-von-Guericke University, Magdeburg, Germany.
  3. Institute of Medical Microbiology, Otto-von-Guericke University, Germany.
  4. Group of Adaptive Immunity, Institute of Molecular Genetics, CAS, Prague, Czech Republic.
  5. Organ-Specific Immune Regulation, Helmholtz-Center of Infection Research (HZI). Braunschweig, Germany.
  6. Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York, United States of America.
  7. Department of Immune Control, Helmholtz-Center of Infection Research (HZI). Braunschweig, Germany.
  8. Leibniz Group 'Dendritic Organelles and Synaptic Function', University Medical Center Hamburg-Eppendorf, Center for Molecular Neurobiology, Hamburg, Germany.

PMID: 27657535 PMCID: PMC5033326 DOI: 10.1371/journal.pone.0162863

Abstract

Transmembrane adaptor proteins (TRAPs) are important organisers for the transduction of immunoreceptor-mediated signals. Prr7 is a TRAP that regulates T cell receptor (TCR) signalling and potently induces cell death when overexpressed in human Jurkat T cells. Whether endogenous Prr7 has a similar functional role is currently unknown. To address this issue, we analysed the development and function of the immune system in Prr7 knockout mice. We found that loss of Prr7 partially impairs development of single positive CD4+ T cells in the thymus but has no effect on the development of other T cell subpopulations, B cells, NK cells, or NKT cells. Moreover, Prr7 does not affect the TCR signalling pathway as T cells derived from Prr7 knockout and wild-type animals and stimulated in vitro express the same levels of the activation marker CD69, and retain their ability to proliferate and activate induced cell death programs. Importantly, Prr7 knockout mice retained the capacity to mount a protective immune response when challenged with Listeria monocytogenes infection in vivo. In addition, T cell effector functions (activation, migration, and reactivation) were normal following induction of experimental autoimmune encephalomyelitis (EAE) in Prr7 knockout mice. Collectively, our work shows that loss of Prr7 does not result in a major immune system phenotype and suggests that Prr7 has a dispensable function for TCR signalling.

Conflict of interest statement

The authors have declared that no competing interests exist.

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