An article published this year in “EUROPEAN JOURNAL OF IMMUNOLOGY” using our “Custom Peptide Production Service” (MOG Peptide), by our customers from Facultad de Medicina (UCLM), Instituto de Investigación en Discapacidades Neurológicas (IDINE), Albacete, 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.
Summary:
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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