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An immune gate of depression – early neuroimmune development in the formation of the underlying depressive disorder

journal contribution
posted on 2019-12-01, 00:00 authored by M Kowalczyk, J Szemraj, K Bliźniewska, M Maes, Michael BerkMichael Berk, K P Su, P Gałecki
© 2019 Institute of Pharmacology, Polish Academy of Sciences The prevalence of depression worldwide is increasing from year to year and constitutes a serious medical, economic and social problem. Currently, despite multifactorial risk factors and pathways contributing to depression development, a significant aspect is attributed to the inflammatory process. Cytokines are considered a factor activating the kynurenine pathway, which leads to the exhaustion of tryptophan in the tryptophan catabolite (TRYCAT) pathway. This results in the activation of potentially neuroprogressive processes and also affects the metabolism of many neurotransmitters. The immune system plays a coordinating role in mediating inflammatory process. Beginning from foetal life, dendritic cells have the ability to react to bacterial and viral antigens, stimulating T lymphocytes in a similar way to adult cells. Cytotoxicity in the prenatal period shapes the predisposition to the development of depression in adult life. Allostasis, i.e. the ability to maintain the body's balance in the face of environmental adversity through changes in its behaviour or physiology, allows the organism to survive but its consequences may be unfavourable if it lasts too long. As a result, Th lymphocytes, in particular T helper 17 cells, which play a central role in the immunity of the whole body, contribute to the development of both autoimmune diseases and psychiatric disorders including depression, as well as have an impact on the differentiation of T CD4+ cells into Th17 cells in the later development of the child's organism, which confirms the importance of the foetal period for the progression of depressive disorders.



Pharmacological reports






1299 - 1307




Amsterdam, The Netherlands





Publication classification

C1 Refereed article in a scholarly journal