12 research outputs found
Microscopy of the bacterial flora on fresh vaginal smears.
Objective: The relationship between pregnancy outcome and expression of the heat shock proteins
(hsps) or hsp-antibody complexes of 60kD (hsp60), 70kD (hsp70), and 90kD (hsp90) in placental tissue and circulating antibodies to hsps was evaluated
Stimulated mast cells promote maturation of myocardial microvascular endothelial cell neovessels by modulating the angiopoietin-Tie-2 signaling pathway
Full-length and truncated neurokinin-1 receptor expression and function during monocyte/macrophage differentiation
In the pubertal rat, the regulation of ovarian function involves the synergic participation of the sensory and sympathetic innervations that arrive at the gonad
Effector T-cell trafficking between the leptomeninges and the cerebrospinal fluid
In multiple sclerosis, brain-reactive T cells invade the central
nervous system (CNS) and induce a self-destructive inflammatory
process. T-cell infiltrates are not only found within the parenchyma
and the meninges, but also in the cerebrospinal fluid (CSF) that
bathes the entire CNS tissue 1,2 . How the T cells reach the CSF,
their functionality, and whether they traffic between the CSF
and other CNS compartments remains hypothetical 3–6 . Here we
show that effector T cells enter the CSF from the leptomeninges
during Lewis rat experimental autoimmune encephalomyelitis
(EAE), a model of multiple sclerosis. While moving through the
three-dimensional leptomeningeal network of collagen fibres in a
random Brownian walk, T cells were flushed from the surface by
the flow of the CSF. The detached cells displayed significantly lower
activation levels compared to T cells from the leptomeninges and
CNS parenchyma. However, they did not represent a specialized
non-pathogenic cellular sub-fraction, as their gene expression
profile strongly resembled that of tissue-derived T cells and they
fully retained their encephalitogenic potential. T-cell detachment
from the leptomeninges was counteracted by integrins VLA-4 and
LFA-1 binding to their respective ligands produced by resident
macrophages. Chemokine signalling via CCR5/CXCR3 and
antigenic stimulation of T cells in contact with the leptomeningeal
macrophages enforced their adhesiveness. T cells floating in the
CSF were able to reattach to the leptomeninges through steps
reminiscent of vascular adhesion in CNS blood vessels, and invade
the parenchyma. The molecular/cellular conditions for T-cell
reattachment were the same as the requirements for detachment
from the leptomeningeal milieu. Our data indicate that the
leptomeninges represent a checkpoint at which activated T cells
are licensed to enter the CNS parenchyma and non-activated T cells
are preferentially released into the CSF, from where they can reach
areas of antigen availability and tissue damage