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End-point effector stress mediators in neuroimmune interactions: their role in immune system homeostasis and autoimmune pathology

  • Immunology in Serbia
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Abstract

Much evidence has identified a direct anatomical and functional link between the brain and the immune system, with glucocorticoids (GCs), catecholamines (CAs), and neuropeptide Y (NPY) as its end-point mediators. This suggests the important role of these mediators in immune system homeostasis and the pathogenesis of inflammatory autoimmune diseases. However, although it is clear that these mediators can modulate lymphocyte maturation and the activity of distinct immune cell types, their putative role in the pathogenesis of autoimmune disease is not yet completely understood. We have contributed to this field by discovering the influence of CAs and GCs on fine-tuning thymocyte negative selection and, in particular, by pointing to the putative CA-mediated mechanisms underlying this influence. Furthermore, we have shown that CAs are implicated in the regulation of regulatory T-cell development in the thymus. Moreover, our investigations related to macrophage biology emphasize the complex interaction between GCs, CAs and NPY in the modulation of macrophage functions and their putative significance for the pathogenesis of autoimmune inflammatory diseases.

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Acknowledgments

We wish to thank our colleagues, Katarina Mitic PhD, Vesna Vujic PhD, Vesna Kovacevi-Jovanovic PhD, Dusko Kosec PhD, Katarina Radojevic PhD and Aleksandra Rauski for valuable help in the research and stimulating discussion of the results that helped us to shape this review. This work was supported by Grant (175050) from the Ministry of Education and Science, Belgrade, Serbia.

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Correspondence to Mirjana Dimitrijevic.

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Mirjana Dimitrijevic, Stanislava Stanojevic, and Gordana Leposavic equally contributed to this work.

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Dimitrijevic, M., Stanojevic, S., Kustrimovic, N. et al. End-point effector stress mediators in neuroimmune interactions: their role in immune system homeostasis and autoimmune pathology. Immunol Res 52, 64–80 (2012). https://doi.org/10.1007/s12026-012-8275-9

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