ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Systemic lack of canonical histamine receptor signaling results in increased resistance to autoimmune encephalomyelitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- In Silico Analysis Highlights Potential Predictive Indicators Associated with Secondary Progressive Multiple Sclerosis.International journal of molecular sciences · 2024Article
- Neuronal activity and remyelination: new insights into the molecular mechanisms and therapeutic advancements.Frontiers in cell and developmental biology · 2023Review
- The Histamine and Multiple Sclerosis Alliance: Pleiotropic Actions and Functional Validation.Current topics in behavioral neurosciences · 2022Article
- Secondary White Matter Injury and Therapeutic Targets After Subarachnoid Hemorrhage.Frontiers in neurology · 2021Review
- Helix 8 is the essential structural motif of mechanosensitive GPCRs.Nature communications · 2019Article
- Type 2 Inflammatory Responses in Autoimmune Demyelination of the Central Nervous System: Recent Advances.Journal of immunology research · 2019Review
- Treatment with anti-FcεRIα antibody exacerbates EAE and T-cell immunity against myelin.Neurology(R) neuroimmunology & neuroinflammation · 2017Article
- Promoting in vivo remyelination with small molecules: a neuroreparative pharmacological treatment for Multiple Sclerosis.Scientific reports · 2017Article
- Lack of Histamine HFrontiers in pharmacology · 2017Article
- [New therapeutic strategies for remyelination in multiple sclerosis].Der Nervenarzt · 2015Article
- International Union of Basic and Clinical Pharmacology. XCVIII. Histamine Receptors.Pharmacological reviews · 2015Review
- Histamine promotes the development of monocyte-derived dendritic cells and reduces tumor growth by targeting the myeloid NADPH oxidase.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Histamine H3 and H4 receptor ligands modify vascular histamine levels in normal and arthritic large blood vessels in vivo.Inflammation · 2015Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Histamine (HA) is a key regulator of experimental allergic encephalomyelitis (EAE), the autoimmune model of multiple sclerosis. HA exerts its effects through four known G-protein-coupled receptors: H1, H2, H3, and H4 (histamine receptors; H(1-4)R). Using HR-deficient mice, our laboratory has demonstrated that H1R, H2R, H3R, and H4R play important roles in EAE pathogenesis, by regulating encephalitogenic T cell responses, cytokine production by APCs, blood-brain barrier permeability, and T regulatory cell activity, respectively. Histidine decarboxylase-deficient mice (HDCKO), which lack systemic HA, exhibit more severe EAE and increased Th1 effector cytokine production by splenocytes in response to myelin oligodendrocyte gp35-55. In an inverse approach, we tested the effect of depleting systemic canonical HA signaling on susceptibility to EAE by generating mice lacking all four known G-protein-coupled-HRs (H(1-4)RKO mice). In this article, we report that in contrast to HDCKO mice, H(1-4)RKO mice develop less severe EAE compared with wild-type animals. Furthermore, splenocytes from immunized H(1-4)RKO mice, compared with wild-type mice, produce a lower amount of Th1/Th17 effector cytokines. The opposing results seen between HDCKO and H1-4RKO mice suggest that HA may signal independently of H1-4R and support the existence of an alternative HAergic pathway in regulating EAE resistance. Understanding and exploiting this pathway has the potential to lead to new disease-modifying therapies in multiple sclerosis and other autoimmune and allergic diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.