ArticleDrug development research2011
The Lymphocyte Potassium Channels Kv1.3 and KCa3.1 as Targets for Immunosuppression.
Article in Drug development research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.
- Therapeutic options for chronic inflammatory demyelinating polyradiculoneuropathy: a systematic review.BMC neurology · 2014Pooled it
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- Spent Coffee Ground Extracts: A Sustainable Source of Antioxidant and Immunomodulatory Bioactives for Managing Lifestyle-Related Chronic Diseases.International journal of molecular sciences · 2026Review
- SARS-CoV-2 Spike Protein S1 Subunit Induces Neuroinflammation Via Microglial Kv1.3 Channel.Biological psychiatry global open science · 2026Article
- The KCa3.1 KCells · 2026Review
- Selective inhibition of mitochondrial Kv1.3 prevents and alleviates multiple sclerosis in vivo.EMBO molecular medicine · 2025Article
- Effects of β-adrenoceptor antagonist and 5-HTThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Early methionine availability attenuates T cell exhaustion.Nature immunology · 2025Article
- Chlorpromazine directly inhibits Kv1.3 channels by facilitating the inactivation of channels.Molecular brain · 2025Article
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- The novel quinoline derivative SKA-346 as a KRSC advances · 2024Article
- Regulation of T Lymphocyte Functions through Calcium Signaling Modulation by Nootkatone.International journal of molecular sciences · 2024Article
- Immunomodulatory effect ofThe journal of venomous animals and toxins including tropical diseases · 2024Article
- Exploring the therapeutic opportunities of potassium channels for the treatment of rheumatoid arthritis.Frontiers in pharmacology · 2024Review
- Microglia as a cellular target of diclofenac therapy in Alzheimer's disease.Therapeutic advances in neurological disorders · 2023Review
- Development and Challenges of Diclofenac-Based Novel Therapeutics: Targeting Cancer and Complex Diseases.Cancers · 2022Review
- Cm28, a scorpion toxin having a unique primary structure, inhibits KV1.2 and KV1.3 with high affinity.The Journal of general physiology · 2022Article
- How the Potassium Channel Response of T Lymphocytes to the Tumor Microenvironment Shapes Antitumor Immunity.Cancers · 2022Review
- Article
- Immunomagnetic separation is a suitable method for electrophysiology and ion channel pharmacology studies on T cells.Channels (Austin, Tex.) · 2021Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The voltage-gated Kv1.3 and the calcium-activated KCa3.1 potassium channel modulate many calcium-dependent cellular processes in immune cells, including T-cell activation and proliferation, and have therefore been proposed as novel therapeutic targets for immunomodulation. Kv1.3 is highly expressed in CCR7(-) effector memory T cells and is emerging as a target for T-cell mediated diseases like multiple sclerosis, rheumatoid arthritis, type-1 diabetes mellitus, allergic contact dermatitis, and psoriasis. KCa3.1 in contrast is expressed in CCR7(+) naïve and central memory T cells, as well as in mast cells, macrophages, dedifferentiated vascular smooth muscle cells, fibroblasts, vascular endothelium, and airway epithelium. Given this expression pattern, KCa3.1 is a potential therapeutic target for conditions ranging from inflammatory bowel disease, multiple sclerosis, arthritis, and asthma to cardiovascular diseases like atherosclerosis and post-angioplasty restenosis. Results from animal studies have been supportive of the therapeutic potential of both Kv1.3 and KCa3.1 blockers and have also not shown any toxicities associated with pharmacological Kv1.3 and KCa3.1 blockade. To date, two compounds targeting Kv1.3 are in preclinical development but, so far, no Kv1.3 blocker has advanced into clinical trials. KCa3.1 blockers, on the other hand, have been evaluated in clinical trials for sickle cell anemia and exercise-induced asthma, but have so far not shown efficacy. However, the trial results support KCa3.1 as a safe therapeutic target, and will hopefully help enable clinical trials for other medical conditions that might benefit from KCa3.1 blockade.
Identifiers
What OpenQuestion holds
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.