Immune Cells Across the Blood Brain Barrier

Migration of Immune Cells Across the Blood Brain Barrier 

Blockade of neutrophil infiltration in experimental stroke models, through inhibition of adhesion molecules (ICAM-1, 

The concept of the neurovascular unit —a functional entity comprising neurons, astrocytes, smooth muscle cells and endothelial cells— has now emerged and it is appreciated that this coordinated unit plays a key role in the hemodynamic response to alterations in brain function and activity. Disruption of this regulatory network occurs after stroke and it is now believed that efforts at neuroprotection should target the entire unit, not just neurons (del Zoppo, 2006). 

Stroke induces an acute stress response—i.e., over-activation of the sympathetic nervous system and increased corticosteroid levels (with resultant neutrophiha and lymphocytopenia). This in turn leads to depressed immunity and altered immune responses during the acute phase of stroke and may predispose patients to infections, particularly pneumonia, which is the commonest cause of mortality after the first few days of stroke (Meisel et al., 2005). In the clinical setting, increased total white cell counts and neutrophilia, which correlate with infarct size, are independently associated with worse outcome after stroke. Recently a massive and early activation of the systemic immnne system has been shown to occur also in experimental stroke (Offner et al., 2006). 

Recently, elevated Cod CD28 T cell connts have been shown to be associated with worse ontcome after ischemic stroke (Nadareishvili et al., 2004). This pro-inflammatory T cell snbset is characterized by longevity, resistance to 

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While the specific mechanisms of action of interferon-pia and interferon-pib in MS are not fully understood, each interferon has a number of immune-mediating activities (see Section 7.1). A recent review article on multiple sclerosis observed The interferons reduce the proliferation of T cells and the production of tumor necrosis factor a, decrease antigen presentation, alter cytokine production to favor ones governed by type 2 helper T (Th2) cells, increase the secretion of interleukin-10, and reduce the passage of immune cells across the blood-brain barrier by means of their effects on adhesion molecules, chemokines, and proteases [2]. 

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