An article published this year in “European Jounal of Immunology” using our “Peptide Production Service (MOG peptide production)”, by our customers from Centro Regional de Investigaciones Biomédicas (CRIB), Albacete, Spain, in the analysis of how Absence of Notch1 in murine myeloid cells attenuates the development of experimental autoimmune encephalomyelitis by affecting Th1 and Th17 priming. Congrats and Thanks.
Summay:
Inhibition of Notch signalling in T cells attenuates
the development of experimental autoimmune encephalomyelitis (EAE), a mouse
model of multiple sclerosis. Growing evidence indicates that myeloid cells are
also key players in autoimmune processes. Thus, the present study evaluates the
role of the Notch1 receptor in myeloid cells on the progression of myelin
oligodendrocyte glycoprotein (MOG)35-55-induced EAE, using mice with a myeloid-specific deletion of
the Notch1 gene
(MyeNotch1KO). We found that EAE progression was less severe in the absence of Notch1 in myeloid
cells. Thus, histopathological analysis revealed reduced pathology in the
spinal cord of MyeNotch1KO mice, with decreased microglia/astrocyte activation,
demyelination and infiltration of CD4+ T cells. Moreover, these mice showed lower Th1 and Th17
cell infiltration and expression of IFN-γ
and IL-17 mRNA in the spinal cord. Accordingly, splenocytes from MyeNotch1KO
mice reactivated in vitro presented reduced Th1 and Th17 activation, and lower
expression of IL-12, IL-23, TNF-α,
IL-6, and CD86. Moreover, reactivated wild-type splenocytes showed increased Notch1 expression,
arguing for a specific involvement of this receptor in autoimmune T cell
activation in secondary lymphoid tissues. In summary, our results reveal a key
role of the Notch1 receptor in myeloid cells for the initiation and progression
of EAE.
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