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Saraiva-Santos, T., Zaninelli, T. H., & Pinho-Ribeiro. (2024). Modulation of host immunity by sensory neurons. Trends in Immunology, 45(5), 381–396. Added by: Dr. Enrique Feoli (28/06/2025, 20:45) Last edited by: Dr. Enrique Feoli (28/06/2025, 20:48) |
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| Resource type: Journal Article DOI: 10.1016/j.it.2024.03.005 ID no. (ISBN etc.): 1471-4906 BibTeX citation key: SaraivaSantos2024 View all bibliographic details  |
Categories: BioAcyl Corp Keywords: cancer, infection, neuro-immune, pathogens Creators: Pinho-Ribeiro, Saraiva-Santos, Zaninelli Collection: Trends in Immunology |
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| Abstract |
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Recent studies have uncovered a new role for sensory neurons in influencing mammalian host immunity, challenging conventional notions of the nervous and immune systems as separate entities. In this review we delve into this groundbreaking paradigm of neuroimmunology and discuss recent scientific evidence for the impact of sensory neurons on host responses against a wide range of pathogens and diseases, encompassing microbial infections and cancers. These valuable insights enhance our understanding of the interactions between the nervous and immune systems, and also pave the way for developing candidate innovative therapeutic interventions in immune-mediated diseases highlighting the importance of this interdisciplinary research field.
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| Notes |
The impact of sensory neurons on host immunity to viruses. (A) Herpes simplex virus type 1 (HSV-1) targets the peripheral nervous system and establishes latent infections in the sensory ganglia. Key viral glycoproteins, including glycoprotein K (gK), interact with receptors on neuron surfaces, facilitating viral fusion and enhancing infectivity. The interaction of neuronal signal peptide peptidase (SPP) with gK in trigeminal ganglia neurons increases HSV-1 latency-reactivation events and CD8+ T cell exhaustion in the ganglion. In addition, calcitonin gene-related peptide (CGRP) inhibits entry receptors and mechanisms used by HSV-1 to infect Langerhans cells. (B) Infectious hematopoietic necrosis virus (IHNV), an aquatic rhabdovirus, engages olfactory sensory neurons (OSNs), triggering immune responses and unconventional CD8+ T cell recruitment. This interaction relies on a distinctive TrkA-sensing mechanism activated by viral G proteins. (C) Within the respiratory tract, the activation of glossopharyngeal GABRA1+ sensory neurons by prostaglandin E2 (PGE2) triggers sickness behavior and exacerbates morbidity in mice infected with influenza virus. Blocking the PGE2 receptor EP3 in these neurons enhances host immunity and survival, reducing viral titers and limiting spread in the tissue. (D) Coinfection of mouse OSNs with attenuated strains of murid herpesvirus 4 (HSV-4) and cytomegalovirus enhances infectivity and virulence through recombination events.
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