MORÓN VÍCTOR GABRIEL
Congresos y reuniones científicas
Título:
LSP1-/- DENDRITIC CELLS INDUCE DEFECTIVE ANTIGEN PRESENTATION TO CD4+ LYMPHOCYTES
Autor/es:
NICOLAS DANIEL DHO; MERCEDES PASCUAL; MARÍA INÉS CRESPO; MARÍA C PISTORESI- PALENCIA; BELKYS A. MALETTO; G MORON
Lugar:
virtual
Reunión:
Congreso; LXVIII REUNIÓN ANUAL DE LA SOCIEDAD ARGENTINA DE INMUNOLOGÍA (SAI); 2020
Institución organizadora:
SOCIEDAD ARGENTINA DE INMUNOLOGÍA (SAI)
Resumen:
Leukocyte-specific protein 1 (LSP1) is a 52 kDa cytoplasmic F-actin
binding phosphoprotein expressed in all human and murine leukocytes
and endothelial cells. LSP1 is an important regulator of actin
cytoskeleton remodelling. We have previously shown that CD4+ T
cells from Lsp1-/- mice have a poorer proliferation than CD4+ T cells
from wild type (WT) mice after antigen exposure in vivo and in vitro
with bone marrow derived dendritic cells (BMDCs).
In order to study the role of LSP1 in DCs to promote a CD4+ T
cell-mediated response, we evaluated the capacity of Lsp1-/- DCs
to present antigens in a context of major histocompatibility complex
class II (MHC II). In vitro, BMDCs were derived from Lsp1-/- mice with
Flt3-L. BMDCs were pulsed with soluble or particulated Ovalbumin
(OVAw or OVAb, respectively), then stimulated with CpG-ODN 1826
and finally cocultured with CD4+ T cells hybridoma (TH3Z OT II). After
an overnight incubation, a significantly lower activation of TH3Z
OT II cells was observed with Lsp1-/- BMDCs incubated with OVAw (p< 0.0001) and OVAb (p< 0.001) compared to Lsp1+/+ BMDCs.
In addition, Lsp1-/- BMDCs show a lower expression of CD40, CD80,
CD86 and MHC II molecules than BMDCs from WT mice after CpGODN
1826 stimulus (p>0.05, p<0.05, p<0.0001, p<0.01 respectively).
These results suggest that LSP1 deficiency affects DC antigen presentation
machinery in MHC II context.
binding phosphoprotein expressed in all human and murine leukocytes
and endothelial cells. LSP1 is an important regulator of actin
cytoskeleton remodelling. We have previously shown that CD4+ T
cells from Lsp1-/- mice have a poorer proliferation than CD4+ T cells
from wild type (WT) mice after antigen exposure in vivo and in vitro
with bone marrow derived dendritic cells (BMDCs).
In order to study the role of LSP1 in DCs to promote a CD4+ T
cell-mediated response, we evaluated the capacity of Lsp1-/- DCs
to present antigens in a context of major histocompatibility complex
class II (MHC II). In vitro, BMDCs were derived from Lsp1-/- mice with
Flt3-L. BMDCs were pulsed with soluble or particulated Ovalbumin
(OVAw or OVAb, respectively), then stimulated with CpG-ODN 1826
and finally cocultured with CD4+ T cells hybridoma (TH3Z OT II). After
an overnight incubation, a significantly lower activation of TH3Z
OT II cells was observed with Lsp1-/- BMDCs incubated with OVAw (p< 0.0001) and OVAb (p< 0.001) compared to Lsp1+/+ BMDCs.
In addition, Lsp1-/- BMDCs show a lower expression of CD40, CD80,
CD86 and MHC II molecules than BMDCs from WT mice after CpGODN
1826 stimulus (p>0.05, p<0.05, p<0.0001, p<0.01 respectively).
These results suggest that LSP1 deficiency affects DC antigen presentation
machinery in MHC II context.
