In spite of many years of research, the pathomechanism of depression has
not yet been elucidated. Among many hypotheses, the immune theory has generated a
substantial interest. Up till now, it has been thought that depression is accompanied
by the activation of inflammatory response and increase in pro-inflammatory cytokine
levels. However, recently this view has become controversial, mainly due to the
family of small proteins called chemokines. They play a key role in the modulation of
peripheral function of the immune system by controlling immune reactions,
mediating immune cell communication, and regulating chemotaxis and cell adhesion.
Last studies underline significance of chemokines in the central nervous system, not
only in the neuromodulation but also in the regulation of neurodevelopmental
processes, neuroendocrine functions and in mediating the action of classical neurotransmitters. Moreover,
it was demonstrated that these proteins are responsible for maintaining interactions between neuronal and
glial cells both in the developing and adult brain also in the course of diseases.
This review outlines the role of chemokine in the central nervous system under physiological and
pathological conditions and their involvement in processes underlying depressive disorder. It summarizes
the most important data from experimental and clinical studies.
Keywords: Antidepressant drugs, chemokine, chemokine receptors, depression, neuroinflammation, neuroplasticity,
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