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Journal of Transmitted Diseases and Immunity
ISSN: 2573-0320 Page 36
Volume 4
May 10-11, 2018
Frankfurt, Germany
Immunology Research 2018
Tissue Science 2018
JOINT EVENT
2 2 n d E d i t i o n o f I n t e r n a t i o n a l C o n f e r e n c e o n
Immunology and
Evolution of Infectious Diseases
&
1 2 t h E d i t i o n o f I n t e r n a t i o n a l C o n f e r e n c e o n
Tissue Engineering and
Regenerative Medicine
Neurons reprogram encephalitogenic T cells (T (enc)) to
become regulatory Treg cells FoxP3+Tregs or FoxA1+Tregs.
We reported previously that neuronal ability to generate
FoxA1+Tregs was central to preventing neuroinflammation in
experimental autoimmune encephalomyelitis (EAE). Mice
lacking the cytokine interferon (IFN)β were defective in
generating FoxA1+Tregs in the brain. Neuron-induced FoxA1+Tregs
were capable of preventing chronic and demyelinating EAE in
mice lacking IFNβ. Here we show that lack of neuronal IFN β-
signaling was associated with lack of neuronal expression
of program death-ligand1 (PDL1), which also prevented their
ability to reprogram Tenc cells to FoxA1+Tregs . Transfer of IFNβ
competent encephalitogenic T cells to mice lacking IFNβ or its
receptor; IFN AR in the brain (NesCre:Ifnarfl/fl) led to the absence
of FoxA1+Tregs generation and aggravated neuroinflammation.
We identified that IFNβ activated neuronal PI3K/Akt signaling.
Phosphorylated Akt consequently bound to transcription
factor FoxA1, which upon translocation to the nucleus induced
neuronal PDL1 expression. Conversely, inhibition of PI3K/Akt,
or FoxA1 and PDL1 knock-down blocked neuronal ability to
generate FoxA1+Tregs. Our study identified crucial molecular
player’s central for neuronal ability to reprogram pathogenic
T-cells and to generate FoxA1+Tregs, which could be a therapeutic
target to prevent neuroinflammation.
Biography
Yawei Liu has a medical doctor background and has been doing medical
research for more than 10 years. Since her Ph.D., she mainly focused on
the role of neurons in the regulation of auto-reactive T cells and central ner-
vous system (CNS) inflammation. We reported a novel function for neurons
as being highly immune-competent cells, based on their crucial role in the
regulation of T-cell responses and CNS inflammation in models of multiple
sclerosis
Neuronal IFN-beta–induced PI3K/Akt-FoxA1 signaling is
essential for generation of FoxA1 +Treg cells
Yawei Liu1, Andrea Marin1, Patrick Ejlerskov1 , Louise Munk Rasmussen1, Mar-
co Prinz2, 3 and Shohreh Issazadeh-Navikas1
1BRIC - University of Copenhagen, Denmark
2Institute for Neuropathology - University of Copenhagen, Germany
3Centre for Biological Signaling Studies - University of Copenhagen, Germany
Yawei Liu et al., J Transm Dis Immun 2018, Volume 2
DOI: 10.21767/2573-0320-C2-005