Abstract
T helper 17 (Th17) cells represent a distinct population of immune cells, important in the defense of the organism against extracellular infectious agents. Because of their cytokine profile and ability to recruit other immune cell types, they are highly pro-inflammatory and are involved in the induction of several autoimmune disorders. Recent studies show that Th17 cells and their signature cytokine IL-17 have also a role in a wide variety of neurological diseases. This review article will briefly summarize the evidence linking Th17 cells to brain diseases associated with cognitive impairment, including multiple sclerosis (MS), ischemic brain injury and Alzheimer’s disease (AD). We will also investigate the mechanisms by which these cells enter the brain and induce brain damage, including direct effects of IL-17 on brain cells and indirect effects mediated through disruption of the blood-brain barrier (BBB), neurovascular dysfunction and gut-brain axis. Finally, therapeutic prospects targeting Th17 cells and IL-17 will be discussed.
Highlights
It is well documented that T helper 17 (Th17) cells are important in the defense of the organism against opportunistic pathogens of fungal or bacterial origin, making them a fundamental part of the adaptive immune system
It has become clear that these cells are involved in the pathogenic mechanism behind several inflammatory disorders, such as multiple sclerosis (MS), inflammatory bowel disease (IBD), rheumatoid arthritis (RA) and psoriasis
Recent evidence provided insight into the trafficking of Th17 cells in and out of the brain and their potential contribution to brain diseases associated with cognitive impairment (Reboldi et al, 2009; Glatigny et al, 2011; Rothhammer et al, 2011; Engelhardt and Ransohoff, 2012)
Summary
It is well documented that T helper 17 (Th17) cells are important in the defense of the organism against opportunistic pathogens of fungal or bacterial origin, making them a fundamental part of the adaptive immune system. Th17 cells play a critical role on mucosal surfaces, such as lung and gut, where they promote the activation of pro-inflammatory danger signals that regulate the recruitment of neutrophils and the expression of anti-microbial factors. The induction of innate immune genes including neutrophil-activating factors, antimicrobial peptides and acute phase proteins allows Th17 cells to execute their defencing functions (Conti et al, 2009). Because of their cytokine profile and ability to recruit other immune cell types, they are extremely pro-inflammatory and are implicated in the induction of several autoimmune diseases (Gaffen, 2009). IL-17 promotes the expression of genes encoding pro-inflammatory and hematopoietic cytokines, chemokines and immune cell chemoattractants, antimicrobial peptides and matrix metalloproteinases (MPOs) from fibroblasts, endothelial cells
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