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For example, the synaptic clearance of GABA and glutamate by these cells is known to influence locomotion.

We have further shown that the insulin produced by these cells is biologically active and induces normoglycemia when injected in diabetic animals.

Synthesis of NO by these cells is stimulated by a variety of signals including hormones, cytokines, growth factors, fluid shear stress, and mechanical loading, resulting in a number of distinct physiological and pathophysiological responses.

Indeed, lactate concentration in culture supernatant was systematically 10-fold higher than lactate concentration measured into lymphocytes, suggesting that the major part of lactate produced by these cells is rapidly secreted in the extracellular milieu.

Moreover, the production of IL-17 by these cells is regulated by both TLR4 and TLR9.

Indeed, mice unable to produce ROI (phox47−/− mice) do not control a secondary L.m infection unless adoptively transferred with Wt neutrophils or inflammatory monocytes, demonstrating that ROI secretion by these cells is required for secondary L.m killing.

Release of insulin by these cells was confirmed by radioimmunoassay.

Growing evidence indicate that trophic factors secreted by these cells are the key mechanism by which they are acting.

The effects of colony-stimulating factors on the platelet-activating factor acetylhydrolase secretion by these cells were examined.

The CD4+CD25high cells were obtained by fluorescence-activated cell sorting and FOXP3 expressed by these cells was >90%.

The innate immune responses mediated by these cells are important for host defense against bacteria and viruses [1], [2].