Resident microglial cell

Figure 44.3. T cell-mediated neui oprotecdon in a PD model. In MPTP-intoxicated mice, regulatory T cells infiltrate tire inflamed nigrostiiatal patliway where tliey encounter cross-reactive CNS antigens (such as myelin basic protein or reactive species-modified proteins) presented in tire context of MHC by resident microglial cells. In response, activated T cells secrete anti-inflammatory cytokines such as IL-4, IL-10, and TGF- 3 tliat suppress toxic microglial activities. Neurotrophin expression may occur directly from T cells or T cell-derived IL-4, and IL-10 may induce neurotrophin production in neigliboimg glia. Tliese activities lead to neuroprotection indirectly by suppression of microglial responses and directly tlu ough tire local delivery of neurotropliins.

A brain macrophage, simply put, is a macrophage in the brain. The normal brain parenchyma is devoid of macrophages they appear only when scavenger cells are needed. There are a number of potential sources of brain macrophages and these include CNS resident microglial cells, blood-borne monocytes, and perivascular and meningeal cells.2... 

Ependymal cells abut layers of astrocytes, which in turn envelop neurons, neurites and vascular components. In addition to neurons and glial cells, such as astrocytes and oligodendrocytes, the normal CNS parenchyma contains blood vessels and microglial cells, the resident macrophages of the CNS. 

Figure 17.47 Comparison of a response to an antigen from a normal Th cell with a Th cell infected with HIV. Thickness of lines indicates extent of the cytokine stimulus. Note that the virus infects peripheral and resident macrophages as well as Th cells and microglial cells in the brain.

In the recent years microglial cells have received a wealth of attention in relation to their role as resident immune cells in the brain (Raivich et al., 1999 Streit, 2002). They are protagonists of the immune surveillance in the CNS, and virtually any inflammatory,... 

A further way to elevate oxidative stress in the brain in neurodegenerative diseases is the activation of microglial cells, the resident macrophages of the brain. These cells are responsible for the removal of aggregated proteins from the brain and are activated by these. Activation of microgha produces large amounts of free radicals [137] that contribute to the burden of oxidative stress in the affected brain. 

The indirect toxicity of both tangles and plaques almost certainly results from inflammation. Plaques and tangles are recognized as alien by the brain s resident inflammatory cells, the microglial cells, which attempt... 

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