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      A Possible Role for Acetylcholine in the Dialogue between Thymocytes and Thymic Stroma

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          In this article we will review data suggesting that acetylcholine takes part in the mutual interplay between developing T cells and thymic epithelium, and thereby may influence the generation of the T-cell repertoire. In the first part we will recapitulate our findings according to which cholinergic agonists affect thymocyte apoptosis via a nicotinergic effect on thymic epithelial cells. In the second part we will present evidence that acetylcholine within the thymus is mainly derived from the thymocytes themselves, and that the production and release of this neurotransmitter is dependent on activation of thymic lymphocytes.

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          Most cited references 3

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          Development in the thymus: it takes two to tango.

          Intrathymic T-cell development is dependent upon signals provided by the thymic stromal cell microenvironment. However, loss of thymic T cells in natural and experimentally induced situations is associated with a reduction in the surrounding epithelium, suggesting an interdependence between thymocytes and their microenvironment. Here, the authors review the evidence in favour of this intrathymic symbiosis, and hypothesize that T cells may provide maturation and survival signals that are necessary for the development and maintenance of their microenvironment.
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            Thymus-derived Glucocorticoids Regulate Antigen-specific Positive Selection

            While it is generally believed that the avidity of the T cell antigen receptor (TCR) for self antigen/major histocompatibility complex (MHC) determines a thymocyte's fate, how the cell discriminates between a stimulus that causes positive selection (survival) and one that causes negative selection (death) is unknown. We have previously demonstrated that glucocorticoids are produced in the thymus, and that they antagonize deletion caused by TCR cross-linking. To examine the role of glucocorticoids during MHC-dependent selection, we examined thymocyte development in organ cultures in which corticosteroid biosynthesis was inhibited. Inhibition of glucocorticoid production in thymi from α/β-TCR transgenic mice resulted in the antigen- and MHC-specific loss of thymocytes that normally recognize self antigen/MHC with sufficient avidity to result in positive selection. Furthermore, inhibition of glucocorticoid production caused an increase in apoptosis only in CD+CD8+ thymocytes bearing transgenic TCRs that recognized self antigen/MHC. These results indicate that the balance of TCR and glucocorticoid receptor signaling influences the antigen-specific thymocyte development by allowing cells with low-to-moderate avidity for self antigen/MHC to survive.
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              Radioimmunoassay for acetylcholine in the rat brain.

              Specific antiserum against acetylcholine (ACh) was produced in the rabbit immunized with a choline hemiglutarate-bovine serum albumin conjugate. The antiserum significantly cross-reacted with choline carboxylates, such as butyrylcholine, succinylcholine, and carbamylcholine. However, neither choline itself nor choline phosphates, such as phosphatidylcholine and phosphorylcholine, showed any significant cross-reaction. The antiserum was used to develop a radioimmunoassay for ACh. The assay can reliably determine as little as 170 pg of ACh. Acetylcholine concentrations in two regions of the rat brain were determined directly from an aqueous extract. After inhibition of acetylcholinesterase with physostigmine, ACh increased more in the forebrain than in the brainstem.

                Author and article information

                S. Karger AG
                April 1999
                08 January 1999
                : 6
                : 1-2
                : 51-55
                aInstitute of General and Experimental Pathology, University of Graz, Austria; bDepartment of Cell Biology, The Weizmann Institute of Science, Rehovot, Israel; cKyoritsu College of Pharmacy, Tokyo, Japan; dInstitute of Pharmaceutical Technology, University of Graz, Austria
                26364 Neuroimmunomodulation 1999;6:51–55
                © 1999 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 3, References: 27, Pages: 5


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