INVESTIGADORES
MORON Victor Gabriel
congresos y reuniones científicas
Título:
MODULATION OF NEUTROPHIL MIGRATORY PATTERN AFTER IMMUNE COMPLEX STIMULATION.
Autor/es:
CAROLINA GORLINO; FLORENCIA HARMAN; ROMINA P. RANOCCHIA; ALEJANDRA GARCÍA; GABRIEL MORÓN; BELKYS MALETTO; PETER HEERINGA; MARÍA C PISTORESI- PALENCIA.
Lugar:
Mar del Plata
Reunión:
Congreso; LX Reunión de la Sociedad Argentina de Inmunología; 2012
Institución organizadora:
Sociedad Argentina de Inmunología
Resumen:
Neutrophils recruited from the blood to inflammatory sites are key
contributors to the nature of an immune response; however, their
presence in chronic inflammatory sites, such as in immune complex
(IC)-mediated autoimmune diseases, can be pathogenic. In this study we
wanted to determine if IC-stimulation could modulate the expression of
migratory molecules and receptors and, hence, drive neutrophil
migration. We showed that after in vitro OVA/anti-OVA IC stimulation,
murine neutrophils downregulated twofold the surface expression of CD62L
(p˂0.05), whereas upregulated twofold their expression of LFA-1
(p˂0.05). Interestingly, IC also induced the expression of the chemokine
receptor CXCR3 on neutrophils (p˂0.05). Additionally, we found that
mRNA expression of sphingosine-1-phosphate (S1P) receptor S1PR4 was
increased threefold in neutrophils stimulated with IC (p˂0.01). In
parallel, we performed flow cytometric analysis in normal human blood
samples to determine if IC could also regulate the expression of these
migratory molecules on human neutrophils. We showed that a subset of
CD16highCD62Llow neutrophils appeared after stimulation with heat
aggregated IgG (HAGG). Moreover, this subpopulation showed to decrease
threefold the expression of CXCR2, while upregulated two- and four-fold
the expression of both CXCR3 and CD54, respectively, in comparison to
the CD16highCD62Lhigh neutrophil subset (p˂0.01). When we investigated
the signal pathways involved in the regulation of the surface expression
of these molecules, we showed that the upregulation of CD54 on
CD16highCD62Llow neutrophils was altered after rapamycin treatment
(p˂0.05), showing that mTOR could be a signal pathway involved in the
modulation of CD54 expression. Taken together, the results presented
here demonstrated that the stimulation with IC modulate the expression
of multiple intercellular adhesion molecules and receptors comprised in
neutrophil trafficking.