ArticleEuropean journal of immunology2012
Combinatorial roles for histamine H1-H2 and H3-H4 receptors in autoimmune inflammatory disease of the central nervous system.
Article in European journal of immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 39 citations in OpenAlex.
- GPCR-Driven Muscarinic M1 and Histamine H1 Receptor Signaling Converging on the PI3K/Akt/mTOR Pathway: Functional Integration in Neuroinflammation and Myelin Repair in Multiple Sclerosis.Molecular neurobiology · 2026Review
- Review
- G Protein-Coupled Receptors in Cerebrovascular Diseases: Signaling Mechanisms and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- The Histamine and Multiple Sclerosis Alliance: Pleiotropic Actions and Functional Validation.Current topics in behavioral neurosciences · 2022Article
- Review
- Histamine Induces Microglia Activation and the Release of Proinflammatory Mediators in Rat Brain Via HJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Article
- Enigmatic Histamine Receptor HLife (Basel, Switzerland) · 2020Review
- Fatigue, Sleep, and Autoimmune and Related Disorders.Frontiers in immunology · 2019Review
- Bone Marrow Myeloid Cells Regulate Myeloid-Biased Hematopoietic Stem Cells via a Histamine-Dependent Feedback Loop.Cell stem cell · 2017Article
- AVN-101: A Multi-Target Drug Candidate for the Treatment of CNS Disorders.Journal of Alzheimer's disease : JAD · 2016Review
- Clemastine Confers Neuroprotection and Induces an Anti-Inflammatory Phenotype in SOD1(G93A) Mouse Model of Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2016Article
- 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
- Focal transient CNS vessel leak provides a tissue niche for sequential immune cell accumulation during the asymptomatic phase of EAE induction.Experimental neurology · 2015Article
- A search for functional histamine H4 receptors in the human, guinea pig and mouse brain.Naunyn-Schmiedeberg's archives of pharmacology · 2015Article
- Histamine induces upregulated expression of histamine receptors and increases release of inflammatory mediators from microglia.Molecular neurobiology · 2014Article
- Histaminergic system in brain disorders: lessons from the translational approach and future perspectives.Annals of general psychiatry · 2014Article
- Expression of histamine receptor genes Hrh3 and Hrh4 in rat brain endothelial cells.British journal of pharmacology · 2013Article
- Cooling treatment transiently increases the permeability of brain capillary endothelial cells through translocation of claudin-5.Neurochemical research · 2013Article
- Systemic lack of canonical histamine receptor signaling results in increased resistance to autoimmune encephalomyelitis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system in which histamine (HA) and its receptors have been implicated in disease pathogenesis. HA exerts its effects through four different G protein-coupled receptors designated H(1)-H(4). We previously examined the effects of traditional single HA receptor (HR) knockouts (KOs) in experimental allergic encephalomyelitis (EAE), the autoimmune model of MS. Our results revealed that H(1) R and H(2) R are propathogenic, while H(3) R and H(4) R are antipathogenic. This suggests that combinatorial targeting of HRs may be an effective disease-modifying therapy (DMT) in MS. To test this hypothesis, we generated H(1) H(2) RKO and H(3) H(4) RKO mice and studied them for susceptibility to EAE. Compared with wild-type (WT) mice, H(1) H(2) RKO mice developed a less severe clinical disease course, whereas the disease course of H(3) H(4) RKO mice was more severe. H(1) H(2) RKO mice also developed less neuropathology and disrupted blood brain barrier permeability compared with WT and H(3) H(4) RKO mice. Additionally, splenocytes from immunized H(1) H(2) RKO mice produced less interferon(IFN)-γ and interleukin(IL)-17. These findings support the concept that combined pharmacological targeting of HRs may be an appropriate ancillary DMT in MS and other immunopathologic diseases.
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