Furthermore, cytokine-driven bystander activation of naive T cells does not contribute to the pool

of Th2 cells. The inflammatory type 2 immune response and the efficiency of worm expulsion were dependent on a broad repertoire of TCR specificities. We thank I. Schiedewitz, A. Turqueti-Neves, C. Schwartz and S. Wirth for technical assistance; BAY 57-1293 S. Huber, A. Turqueti-Neves and C. Schwartz for critical comments; A. Bol and W. Mertl for animal husbandry and A. Oxenius for providing Smarta mice. This work was supported by the Emmy Noether Program of the Deutsche Forschungsgemeinschaft (Vo944/2-2). The authors have not conflict of interest to declare. “
“Microglia cells, the resident innate immune cells in the brain, are highly active, extending and retracting BMS-777607 cell line highly motile processes through which they continuously

survey their microenvironment for ‘danger signals’ and interact dynamically with surrounding cells. Upon sensing changes in their central nervous system microenvironment, microglia become activated, undergoing morphological and functional changes. Microglia activation is not an ‘all-or-none’ process, but rather a continuum depending on encountered stimuli, which is expressed through a spectrum of molecular and functional phenotypes ranging from so-called ‘classically activated’, with a highly pro-inflammatory profile, to ‘alternatively activated’ associated with a beneficial, less inflammatory, neuroprotective profile. Microglia activation has been demonstrated in most neurological diseases of diverse aetiology and has been implicated as a contributor to neurodegeneration. The possibility to promote microglia’s neuroprotective phenotype has therefore become a therapeutic goal. We have focused our discussion on the role of microglia in multiple

sclerosis, a prototype of inflammatory, demyelinating, neurodegenerative disease, and on the effect of currently approved or on-trial anti-inflammatory therapeutic strategies that might mediate neuroprotection at least in part ZD1839 research buy through their effect on microglia by modifying their behaviour via a switch of their functional phenotype from a detrimental to a protective one. In addition to pharmaceutical approaches, such as treatment with glatiramer acetate, interferon-β, fingolimod or dimethyl fumarate, we address the alternative therapeutic approach of treatment with mesenchymal stem cells and their potential role in neuroprotection through their ‘calming’ effect on microglia. Microglia, the resident innate immune cells in the brain, represent the first line of defence against exogenous and endogenous threats to the central nervous system (CNS). Microglia are believed to derive from progenitors of mesodermal/mesenchymal origin migrated from the periphery in early postnatal development. In the normal healthy CNS, microglia display a so-called ‘resting’ phenotype, characterized by a typical ramified morphology, a slow turnover rate and low expression of surface molecules.