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Calcitonin gene-related peptide sustains CD8+ T cell inflammatory reactions in drug -induced reactions [scRNA-Seq]

ABSTRACT: We investigated the differentiation pattern of CD8+ T cells from healthy controls and patients with SJS/TEN.

ORGANISM(S): Homo sapiens

PROVIDER: GSE249525 | GEO | 2025/03/31

REPOSITORIES: GEO

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Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-03-31 | GSE249576 | GEO

Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions [CD8 Smart-seq]

Project description:We investigated the differentiation pattern induced by CGRP on CD8+ T cells

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Calcitonin gene-related peptide sustains CD8+ T cell inflammatory reactions in drug -induced reactions [scRNA-Seq]

Project description:Calcitonin gene-related peptide sustains CD8+ T cell inflammatory reactions in drug -induced reactions [scRNA-Seq]

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Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions

Project description:Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions

| PRJNA1049746 | ENA

Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions [CD8 Smart-seq]

Project description:Calcitonin gene-related peptide sustains CD8 T cell inflammatory reactions in drug -induced reactions [CD8 Smart-seq]

| PRJNA1047005 | ENA

Homo sapiens

Project description:PBMS cells from SJS/TEN

| PRJNA114649 | ENA

The Calcitonin/Calcitonin Gene-Related Peptide Family in Invertebrate Deuterostomes.

Project description:Calcitonin (CT)/CT gene-related peptide (CGRP) family peptides (CT/CGRP family peptides) including CT, CGRP, adrenomedullin, amylin, and CT receptor-stimulating peptide have been identified from various vertebrates and perform a variety of important physiological functions. These peptides bind to two types of receptors including CT receptor (CTR) and CTR-like receptor (CLR). Receptor recognition of CT/CGRP family peptides is determined by the heterodimer between CTR/CLR and receptor activity-modifying protein (RAMP). Comparative studies of the CT/CGRP family have been exclusively performed in vertebrates from teleost fishes to mammals and strongly manifest that the CGRP family system containing peptides, their receptors, and RAMPs was derived from a common ancestor. In addition, CT/CGRP family peptides and their receptors are also identified and inferred from various invertebrate species. However, the evolutionary process of the CT/CGRP family from invertebrates to vertebrates remains enigmatic. In this review, I principally summarize the CT/CGRP family peptides and their receptors in invertebrate deuterostomes, highlighting the study of invertebrate chordates including ascidians and amphioxi. The CT/CGRP family peptide that shows similar molecular structure and function with that of vertebrate CT has been identified from ascidian, Ciona intestinalis. Amphioxus, Branchiostoma floridae also possessed three CT/CGRP family peptides, one CTR/CLR receptor, and three RAMP-like proteins. The molecular function of the receptor complex formed by amphioxus CTR/CLR and a RAMP-like protein was clarified. Moreover, CT/CGRP family peptides have been identified in the superphylum Ambulacraria, which is close to Chordata. Finally, this review provides potential hypotheses of the evolution of CGRP family peptides and their receptors from invertebrates to vertebrates.

| S-EPMC6283891 | biostudies-literature

Keratinocyte expression of calcitonin gene-related peptide ?: implications for neuropathic and inflammatory pain mechanisms.

Project description:Calcitonin gene-related peptide (CGRP) is a vasodilatory peptide that has been detected at high levels in the skin, blood, and cerebrospinal fluid (CSF) under a variety of inflammatory and chronic pain conditions, presumably derived from peptidergic C and A? innervation. Herein, CGRP immunolabeling (IL) was detected in epidermal keratinocytes at levels that were especially high and widespread in the skin of humans from locations afflicted with postherpetic neuralgia (PHN) and complex region pain syndrome type 1 (CRPS), of monkeys infected with simian immunodeficiency virus, and of rats subjected to L5/L6 spinal nerve ligation, sciatic nerve chronic constriction, and subcutaneous injection of complete Freund's adjuvant. Increased CGRP-IL was also detected in epidermal keratinocytes of transgenic mice with keratin-14 promoter driven overexpression of noggin, an antagonist to BMP-4 signaling. Transcriptome microarray, quantitative Polymerase Chain Reaction (qPCR), and Western blot analyses using laser-captured mouse epidermis from transgenics, monolayer cultures of human and mouse keratinocytes, and multilayer human keratinocyte organotypic cultures, revealed that keratinocytes express predominantly the beta isoform of CGRP. Cutaneous peptidergic innervation has been shown to express predominantly the alpha isoform of CGRP. Keratinocytes also express the cognate CGRP receptor components, Calcitonin receptor-like receptor (CRLR), Receptor activity-modifying protein 1 (RAMP1), CGRP-receptor component protein (RCP) consistent with known observations that CGRP promotes several functional changes in keratinocytes, including proliferation and cytokine production. Our results indicate that keratinocyte-derived CGRP? may modulate epidermal homeostasis through autocrine/paracrine signaling and may contribute to chronic pain under pathological conditions.

| S-EPMC3157543 | biostudies-literature

The anti-inflammatory regulation of calcitonin gene-related peptide in mouse Aspergillus fumigatus keratitis.

Project description:AIM:To analyze the impact of calcitonin gene-related peptide (CGRP) in mouse keratitis after Aspergillus fumigatus (A. fumigatus) infection. METHODS:C57BL/6 mice were treated subconjunctivally with different concentrations of exogenous CGRP, and BALB/c mice were treated with CGRP8-37 (a CGRP antagonist) before corneas were infected with A. fumigatus. The cornea was assessed under the slit-lamp and the clinical score was recorded. The mRNA levels of IL-1?, TNF-?, IL-6, and MIP-2 were detected by quantitative real-time polymerase chain reaction (PCR), while the protein level of IL-1? was determined by Western blotting. In vitro, RAW264.7 cells were used to investigate NLRP3 and IL-1? expression induced by A. fumigatus after the pretreatment of exogenous CGRP or CGRP8-37. Cytokines expression in RAW264.7 cells was evaluated by real-time PCR and Western blotting. RESULTS:Using exogenous CGRP resulted in down-regulated synthesis of IL-1? and MIP-2 stimulated by A. fumigatus in C57BL/6 mice keratitis, and the synthesis of IL-1?, MIP-2 and IL-6 was up-regulated in BALB/c mice corneas after the pretreatment with CGRP8-37. Pretreatment with exogenous CGRP and CGRP8-37 did not influence TNF-? mRNA levels either in BALB/c or C57BL/6 mice keratitis. The levels of NLRP3 and IL-1? were both reduced in A. fumigatus stimulated-macrophages after treatment with exogenous CGRP. And CGRP8-37 pretreatment would increase NLRP3 and IL-1? levels. CONCLUSION:CGRP may alleviate the inflammatory reaction in mice keratitis after infection with A. fumigatus. The anti-inflammatory effect may be related to the inhibition of NLRP3 expression by CGRP.

| S-EPMC7201344 | biostudies-literature

SJS blister cells

Project description:Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening adverse drug reactions characterized by massive epidermal necrosis, in which the specific danger signals involved remain unclear. Here we show that blister cells from skin lesions of SJS-TEN primarily consist of cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells, and both blister fluids and cells were cytotoxic. Gene expression profiling identified granulysin as the most highly expressed cytotoxic molecule, confirmed by quantitative PCR and immunohistochemistry. Granulysin concentrations in the blister fluids were two to four orders of magnitude higher than perforin, granzyme B or soluble Fas ligand concentrations, and depleting granulysin reduced the cytotoxicity. Granulysin in the blister fluids was a 15-kDa secretory form, and injection of it into mouse skin resulted in features mimicking SJS-TEN. Our findings demonstrate that secretory granulysin is a key molecule responsible for the disseminated keratinocyte death in SJS-TEN and highlight a mechanism for CTL- or NK cell—mediated cytotoxicity that does not require direct cellular contact.

2008-12-04 | GSE13726 | GEO