Biology subjects

Inclan Rico, J.

Publications and source records attributed to Inclan Rico, J..

2 recordsLinked to original sources

bioRxiv2026

Sensory neurons shape γδ T cell effector programs to control Psoriasiform Inflammation.

Psoriasis is a chronic autoimmune skin disorder marked by IL-17 producing gamma delta T cell ({gamma}{delta}T17) and pruritus, but immunoregulatory roles of itch-inducing neurons in this context remain unclear. This study addressed whether non-peptidergic (NP) afferents bearing the Mas-related G protein-coupled receptor D (MrgprD/NP1) and MrgprA3/NP2 subsets had differential effects on psoriasiform immunopathology. Data show human NP1 and NP2 neurons basally expressed an array of pattern recognition and cytokine receptor genes and psoriatic human skin had a profound dysregulation of neuropeptides and their receptors. In mice, imiquimod (IMQ) application reduced the density of MrgprD+ skin afferents, whereas NP1 neuron ablation exacerbated IMQ-induced disease. Strikingly, NP1 activation using either optogenetics or {beta}-alanine before IMQ exposure significantly reduced epidermal thickness, psoriatic clinical score and {gamma}{delta}T17 cell accumulation. In stark contrast, NP2 activation increased the numbers of {gamma}{delta}T17 cells that co-expressed amphiregulin (Areg) and exacerbated IMQ-driven skin pathology. Instead, pre-emptive NP1 stimulation shifted {gamma}{delta} T cell profiles away from being IL-17 and Areg dominant to IL-13+ {gamma}{delta} T cells expressing the transcription factor GATA3 accompanied by IL-10 secretion. Importantly, IL-10 signaling blockade reversed NP1-mediated suppression of IMQ-induced dermatitis. These data show that inflammatory skin disease can be distinctly modulated by sensory neuron subsets.

immunology↗

bioRxiv2025

TRPV1+ neurons promote cutaneous immunity against Schistosoma mansoni.

Immunity against skin-invasive pathogens requires mechanisms that rapidly detect, repel or immobilize the infectious agent. While bacteria often cause painful cutaneous reactions, host skin invasion by the human parasitic helminth Schistosoma mansoni often goes unnoticed. This study investigated the role of pain-sensing skin afferents that express the ion channel Transient Receptor Potential Vanilloid 1 (TRPV1) in the detection and initiation of skin immunity against S. mansoni. Data show that mice infected with S. mansoni have reduced behavioral responses to painful stimuli and sensory neurons exposed from infected mice have significantly less calcium influx and neuropeptide release in response to the TRPV1 agonist capsaicin. Using both gain- and loss-of-function approaches, data show that TRPV1+ neurons are critical regulators of S. mansoni survival during migration from the skin into the pulmonary tract. Moreover, TRPV1+ neurons were both necessary and sufficient to promote proliferation and cytokine production from dermal {gamma}{delta} T cells as well as neutrophil and monocyte skin accumulation post-infection. These results suggest a model in which S. mansoni may have evolved to inhibit TRPV1+ neuron activation as a countermeasure that limits IL-17-mediated inflammation, facilitating systemic dissemination and chronic parasitism. One sentence summaryThe parasitic helminth Schistosoma mansoni averts IL-17-dependent protective immunity by suppressing skin-innervating TRPV1+ neurons.

immunology↗