% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Walker:140384,
author = {Walker, Tara and Schallenberg, Sonja and Rund, Nicole and
Grönnert, Lisa and Rust, Ruslan and Kretschmer, Karsten and
Kempermann, Gerd},
title = {{T} {L}ymphocytes {C}ontribute to the {C}ontrol of
{B}aseline {N}eural {P}recursor {C}ell {P}roliferation but
{N}ot the {E}xercise-{I}nduced {U}p-{R}egulation of {A}dult
{H}ippocampal {N}eurogenesis.},
journal = {Frontiers in immunology},
volume = {9},
issn = {1664-3224},
address = {Lausanne},
publisher = {Frontiers Media},
reportid = {DZNE-2020-06706},
pages = {2856},
year = {2018},
abstract = {Cross-talk between the peripheral immune system and the
central nervous system is important for physiological brain
health. T cells are required to maintain normal baseline
levels of neural precursor proliferation in the hippocampus
of adult mice. We show here that neither T cells, B cells,
natural killer cells nor natural killer T cells are required
for the increase in hippocampal precursor proliferation that
occurs in response to physical exercise. In addition, we
demonstrate that a subpopulation of T cells, regulatory T
cells, is not involved in maintaining baseline levels of
neural precursor proliferation. Even when applied at
supraphysiological numbers, populations of both naive and
stimulated lymphocytes had no effect on hippocampal
precursor proliferation in vitro. In addition, physical
activity had no effect on peripheral immune cells in terms
of distribution in the bone marrow, lymph nodes or spleen,
activation state or chemokine receptor (CXCR4 and CCR9)
expression. Together these results suggest that lymphocytes
are not involved in translating the peripheral effects of
exercise to the neurogenic niche in the hippocampus and
further support the idea that the exercise-induced
regulation of adult neurogenesis is mechanistically distinct
from its baseline control.},
keywords = {Animals / B-Lymphocytes: immunology / B-Lymphocytes:
metabolism / Cell Proliferation / Hippocampus: cytology /
Hippocampus: immunology / Killer Cells, Natural: immunology
/ Killer Cells, Natural: metabolism / Mice, Inbred C57BL /
Mice, Knockout / Mice, Transgenic / Neural Stem Cells:
immunology / Neural Stem Cells: metabolism / Neurogenesis:
immunology / Physical Conditioning, Animal: physiology /
T-Lymphocytes: immunology / T-Lymphocytes: metabolism /
T-Lymphocytes, Regulatory: immunology / T-Lymphocytes,
Regulatory: metabolism / Up-Regulation},
cin = {AG Kempermann 1},
ddc = {610},
cid = {I:(DE-2719)1710001},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342)},
pid = {G:(DE-HGF)POF3-342},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30619254},
pmc = {pmc:PMC6297802},
doi = {10.3389/fimmu.2018.02856},
url = {https://pub.dzne.de/record/140384},
}