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Susan Legg. The presence of AChR in normal rodent and human lymphocytes was confirmed in numerous binding studies using radiolabeled ACh, nicotine and specific muscarinic or nicotinic antagonists reviewed in Kawashima and Fujii, Such radioligands, however, are not selective for special receptor subtypes. Although, the presence of at least some mAChR and nAChR subtypes was detected in all samples, the expression pattern varied significantly among individuals.

These data evidenced the diversity of cholinergic system in human immune cells, where each person may respond to ACh stimulation in a different way. It was proposed that the expression pattern may be genetically determined or regulated by some factors such as infection and physiological stress Kawashima and Fujii, The latter, as shown in mice with a null mutation for a single nAChR subunit, also label collateral targets, with a level of immunoreactivity very similar to wild type Moser et al.

Plasticity of the T-cell cholinergic receptors during differentiation was also demonstrated in murine model Qian et al. It is well-known that nAChR form ligand ACh and nicotine - gated cation channels in neurons and muscles. To better understand the physiological significance of these receptors in lymphocytes, single-cell records were attempted on both B and T subsets using standard patch-clamp techniques Peng et al. However, lymphocytes recordings did not show any current response to a stimulation with ACh, nicotine or cholinergic receptor agonist carbachol.

Then, nAChR may have a different mode of action in lymphocytes Peng et al. Although the underlying mechanisms are not well-understood, there is little doubt about the functionality of activated AChR in lymphocytes.

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Nicotine regulates cell proliferation, differentiation, migration, cell—cell interactions, and apoptosis De Rosa et al. However, there is as yet no in vivo direct evidence demonstrating that T cell- derived ACh binds to AChR on the same cell or neighboring cells, to exert this modulating effect. Principle target of CN is NFATs, heavily phosphorylated at the rest; its dephosphorylation make it permeable via nuclear pore.

By entering nucleus, NFAT induces the transcription of several genes. The cholinergic anti-inflammatory pathway, also termed as inflammatory reflex, together with anti-inflammatory cytokines, glucocorticoids, and other humoral mediators, is involved in the suppression of inflammatory response Tracey, An excellent critical review highlighting the evolution in the understanding of underlying mechanisms was published recently Martelli et al.

Here, we only briefly present this well-studied example, to emphasize the potential of the T cell NNCS in mammal physiology. During the inflammation, pro-inflammatory cytokines activate afferent sensory neurons, which represent the sensory arc of the inflammatory reflex. Axons traveling in the vagus nerve transmit this information as action potentials to the brain stem. The brain stem generates inhibitory signals, which traverse the efferent vagus nerve into the spleen.

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This efferent arc actually represents a cholinergic anti-inflammatory pathway. Electrical stimulation of splenic nerve was believed to result in release of ACh into splenic tissue and into the effluent splenic vein, with a subsequent down regulation of the inflammatory cytokines Tracey, Rosas-Ballina et al.

Using a murine model, they demonstrated that ACh was produced by a subset of T lymphocytes, present in the spleen Rosas-Ballina et al. Consequently, in nude mice, lacking functional T cells, vagal stimulation had no anti-inflammatory effect, whereas it was restored by the adoptive transfer of ACh-synthesizing T lymphocytes Rosas-Ballina et al. In this way, the production of ACh by T cells provides a reliable protective mechanism from inflammatory damage in mammals.

NFAT dephosphorylation and translocation to nucleus as well as the activation of PKC and MAPK cascades culminate in changes of the transcriptional activity and proliferation of an antigen-specific clone Lichtman et al. Activation of these receptors has been linked to the control of MAPK and, as a consequence, to the regulation of cell growth and proliferation Gutkind, ; Gudermann et al. T leukemogenesis is a multistep process, where genetic aberrations during the T cell maturation convert healthy T cell progenitors into leukemic cells that are unable to differentiate, but demonstrate high potential of self-renewal and proliferation.

Due to multiple mutations, T-ALL are heterogeneous and multiclonal. Molecular basis of T-ALL pathogenesis is a subject of intensive studies and is reviewed exhaustively elsewhere Graux et al. This mechanism may be retained in aberrant leukemic progenitors, and involved in the maintenance of an increased proliferation level.

In this chapter we will first provide a summary on the expression and function of cholinergic elements in tumors of different origin, and then present the data, available for T-ALL. We will also discuss a possible relation between genetic aberrations and cholinergic machinery during T leukemogenesis.

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An enhanced level of choline uptake and metabolism is obviously required for actively proliferating tissues, because choline is needed for a rapid biosynthesis of cell membranes. Elevated concentrations of choline and its metabolites were revealed by means of MRS in a wide variety of malignances reviewed in Inazu, Accelerated choline metabolism was considered as a metabolic hallmark that is associated with malignant progression reviewed in Glunde et al.

Nowadays, MRS method which determines elevated local concentrations of choline and its metabolites is widely used to assist the diagnosis and staging of cancer, and evaluate the therapeutic response Hara et al. Several excellent reviews regarding involvement of NNCS in tumorigenesis have been published recently Spindel, ; Russo et al.