III. Symposium of the "German Endocrine Brain Immune Network"
29th September - 2nd October 2003
Psychiatric Hospital, Ludwig-Maximilian University Munich
Nußbaumstraße 7, D-80336 Munich, Germany


A special retrospective for the educational short course can be found here.  

The German Brain Endocrine Immune Network (GEBIN) met up in Munich, 30th September – 2nd October 2003. Thanks to the organizers N. Müller and M. Schwarz, Munich, this 3rd Meeting of GEBIN was again a highlight in this interdisciplinary field of research. Approximately 100 international and national scientists from 12 different research disciplines participated. Similarly as during earlier meetings of the GEBIN in Regensburg and Essen, the program was subdivided into the following parts: 1) Neuro-endocrino-immune Interactions in Neurology, 2) Neuro-endocrino-immune Interactions in Psychiatry, 3) Peripheral Neuroimmune Interactions, 4) Neuroendocrinology and Immune Function, 5) Stress, Behaviour, and Immune Function. In every section, a speaker with a strong international standing presented a review lecture of outstanding quality: 1) Recent advances in neuroimmunology of multiple sclerosis, R. Hohlfeld, Munich, 2) The role of viral infections during neurodevelopment in schizophrenia pathogenesis, P.D. Pearce, Atlanta, 3) Th1 and Th2 immune responses in the periphery activate distinct neuronal pathways in the CNS, G.A.W. Rook, London, 4) Inflammatory control of the hypothalamus-pituitary-adrenal axis, A.B. Grossman, London, 5) Stress, behaviour and immune function – a review on exercise and immunity, B.K. Pedersen, Kopenhagen. In addition, a total of 37 oral short presentations and 38 posters were presented. A poster session with two chairmen guaranteed a good attendance and a lively discussion in front of the posters.

From the personal view point of the author, the following subjects were particularly interesting on this 3rd GEBIN symposium: B. Fellerhoff, Munich, extended her earlier findings that carriers of the TAP1*A!/TAP1*B1 genotype have a 14.7 fold increased relative risk to develop schizophrenia, which supports the idea of a microbiologically triggered pathogenesis of schizophrenia. H. Vedder, Marburg, demonstrated a cortisol-induced increase of TNF from PBMNC in the presence of a mineralocorticoid receptor antagonist. This may shed a completely new light on the intracellular interaction of these two steroid receptors in peripheral immune cells. G.A.W. Rook, London, demonstrated that specific Th1 and Th2 immune response inducing antigens, locally applied to the bronchial epithelium, evoke completely different activation patterns in CNS nuclei as detected by up-regulated fos expression. U. Gimsa, Rostock, reported that typical T cell responses against CNS autoantigens are inhibited by upregulation of CTLA-4 on astrocytes. T. Gebhard, Hannover, demonstrated beta2-adrenergically mediated inhibition of mast cell function. Y. Li, Marburg, showed that primary sensory afferent neurons in dorsal root ganglia may function as endotoxin sensors because he demonstrated that these cells are equipped with the TLR4 receptor. U. Renner, Munich, supported the ubiquitous role of TLR4 as an endotoxin receptor in the neuroendocrine system by demonstrating its presence and function in pituitary cells. L.E. Miller, Regensburg, demonstrated the presence of a sympathetic nerve repellent factor semaphorin 3C in inflamed synovial tissue of patients with rheumatoid arthritis. Presence of this repellent factor may well contribute to the known loss of sympathetic nerve fibres in inflamed synovial tissue. C. Mahuad, Buenos Aires, supported the idea of an increase of cortisol relative to adrenal androgens in patients with tuberculosis. Similar findings were presented in chronic inflammatory diseases, which is thought to add to the chronic inflammatory nature of these diseases. B.K. Pedersen highlighted the role of IL-6 which is up-regulated and secreted from exercising muscle. IL-6 in this sense is a hormone rather than a cytokine. C. Kiank, Greifswald, supported the immune system inhibiting effect of stressful manipulations in mice leading to an improvement of endotoxin-induced mortality. S. Dimitrov, Lübeck, showed the Th1 immune response – favouring effect of night sleep. M.-B. Niemi, Essen, delineated that chemical deletion of important cortical brain areas abrogated immune conditioning. This is the first report which showed a role of the CNS for the well-known conditioning of the immune system. As in earlier years, this meeting illustrated that interdisciplinary research between immunology, endocrinology, and neuroscience in a system biologic manner yields a surplus value in order to unravel the complexity of nature. The next meeting of the GEBIN will take place in 2005. The interested reader may find more information about this, earlier, and future meetings under

Letzte Änderung, 11.2003, Rainer H. Straub