IRIBARREN PABLO
Congresos y reuniones científicas
Título:
Participation of type I-II IFNs in the regulation of the CNS immune surveillance after systemic inflammation
Autor/es:
PERALTA RAMOS, JM; BUSSI, C; ARROYO, DS; IRIBARREN, P
Lugar:
Mar del Plata
Reunión:
Congreso; LXIV reunion anual. Sociedad Argentina de Inmunologia (SAI) SAIC; 2016
Institución organizadora:
SAI - SAIC
Resumen:
Brain-resident microglia (Mi) and peripheral recruited
leukocytes, play essential roles in shaping the immune
response in the central nervous system (CNS). These
cells activate and migrate in response to chemokines
produced during active immune responses and may contribute
to the progression of neuroinflammation. Recent findings have revealed distinct roles for type I (α and β)-II
(γ) interferons (IFNs) in the recruitment of immune cells to
the CNS and highlighted the importance of this process
for brain protection/repair. In this study, we assessed
the participation of type I-II IFNs in the innate immune
response displayed by tissue-resident microglia and recruited inflammatory leukocytes, to better understand
the contribution of these cytokines in the establishment
and development of a neuroinflammatory process induced
by systemic TLR4 stimulation. We characterized the molecular
and cellular players involved in neuroinflammation
induced by i.p. administration of lipopolysaccharide (LPS
- 1.6 mg/kg) to IFN-γ-/- and IFNAR-/- C57BL/6 mice, using
flow cytometry combined with confocal microscopy. Following
stimulation with LPS, we didn´t find any variation
of CD11b+CD45lo microglial cells; however, we noticed
a decrease of CD11b+CD45hi (Ly6Chi/CD11c+) myeloid
recruited leukocytes in both KO mice strains compared to their WT-treated counterparts (p<0.05). Unexpectedly, no
significant changes were observed neither in the absolute
number of MHC-II+ cells nor in the MFI of Mi and peripheral
leukocytes. Interestingly, we found an increase of
CD11b+CD45hiLy6C+Ly6G+ neutrophils from LPS primed
IFNAR-/- mice in comparison with their IFN-γ-/- littermates
(p<0.05). Thereby, IFNs could prove to be important players
in the regulation of leukocyte recruitment to the CNS
by controlling the innate immune response in neuroinflammation.
Furthermore, these findings highlight the ability
of a systemic TLR4-mediated challenge to signal to the
CNS and alter brain´s primary immunity.
leukocytes, play essential roles in shaping the immune
response in the central nervous system (CNS). These
cells activate and migrate in response to chemokines
produced during active immune responses and may contribute
to the progression of neuroinflammation. Recent findings have revealed distinct roles for type I (α and β)-II
(γ) interferons (IFNs) in the recruitment of immune cells to
the CNS and highlighted the importance of this process
for brain protection/repair. In this study, we assessed
the participation of type I-II IFNs in the innate immune
response displayed by tissue-resident microglia and recruited inflammatory leukocytes, to better understand
the contribution of these cytokines in the establishment
and development of a neuroinflammatory process induced
by systemic TLR4 stimulation. We characterized the molecular
and cellular players involved in neuroinflammation
induced by i.p. administration of lipopolysaccharide (LPS
- 1.6 mg/kg) to IFN-γ-/- and IFNAR-/- C57BL/6 mice, using
flow cytometry combined with confocal microscopy. Following
stimulation with LPS, we didn´t find any variation
of CD11b+CD45lo microglial cells; however, we noticed
a decrease of CD11b+CD45hi (Ly6Chi/CD11c+) myeloid
recruited leukocytes in both KO mice strains compared to their WT-treated counterparts (p<0.05). Unexpectedly, no
significant changes were observed neither in the absolute
number of MHC-II+ cells nor in the MFI of Mi and peripheral
leukocytes. Interestingly, we found an increase of
CD11b+CD45hiLy6C+Ly6G+ neutrophils from LPS primed
IFNAR-/- mice in comparison with their IFN-γ-/- littermates
(p<0.05). Thereby, IFNs could prove to be important players
in the regulation of leukocyte recruitment to the CNS
by controlling the innate immune response in neuroinflammation.
Furthermore, these findings highlight the ability
of a systemic TLR4-mediated challenge to signal to the
CNS and alter brain´s primary immunity.
