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Updated: Apr 23, 2026

Development of Recombinant Proteins to Treat Chronic Pain
Published on: April 11, 2018
Lymphotoxin-beta receptor controls the development of chronic pain
Alexei V Tumanov1, Jennifer M Mecklenburg2, Sergei Belugin2
1Department of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
None:
Preventing the development of chronic pain is crucial to avoiding difficult-to-manage, debilitating pain conditions. Our research identifies the lymphotoxin beta receptor (LTβR) as a peripheral master regulator in this process. Activation of LTβR induces mechanical allodynia and increases sensory neuron excitability by engaging peripheral non-neuronal cells, including macrophages and stromal cells. Conversely, local blockade of LTβR reduces neuronal hyperexcitability and irreversibly prevents chronic pain in a neuropathic preclinical model. These LTβR effects are driven by both LTβ and LIGHT. Transcriptomic analysis reveals that LTβR regulates the development of chronic pain by coordinating a peripheral gene-plasticity network that involves immune-related genes and diverse cell types. Overall, LTβR acts as a master regulator controlling the development of pain chronicity by shaping a peripheral gene plasticity network that drives sensory neuronal sensitization.
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