Key result
Extracellular nucleotides and adenosine play opposing roles in multiple sclerosis, with nucleotides activating proinflammatory P2 receptors and adenosine exerting anti-inflammatory effects via P1 receptors.
This review highlights the opposing roles of extracellular nucleotides and adenosine in neuroinflammation, suggesting purinergic signaling pathways as potential therapeutic targets or biomarkers for multiple sclerosis.
Purinergic P2/P1 modulation may guide neuroinflammation therapies; leaves open targeted clinical validation.
Extracellular nucleotides and adenosine play important roles in inflammation. These signaling molecules interact with the cell-surface-located P2 and P1 receptors, respectively, that are widely distributed in the central nervous system and generally exert opposite effects on immune responses. Indeed, extracellular ATP, ADP, UTP, and UDP serve as alarmins or damage-associated molecular patterns that activate mainly proinflammatory mechanisms, whereas adenosine has potent anti-inflammatory and immunosuppressive effects. This review discusses the actual and potential role of extracellular nucleotides and adenosine in multiple sclerosis (MS).
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Cieślak et al. (2011) conducted a review in Multiple sclerosis. Extracellular nucleotides and adenosine was evaluated. Extracellular nucleotides and adenosine play opposing roles in multiple sclerosis, with nucleotides activating proinflammatory P2 receptors and adenosine exerting anti-inflammatory effects via P1 receptors.
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