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This section gives an overview of the disease, and where available shows the following:
More information can be found in the help pages.
✖Disease ID: | 105 | |
Name: | Autoimmune disease | |
Associated with: | 1 target |
Click on the target name to link to its detailed view page
Where available, information is display on the role of the target in the disease; drugs which target the disease and their therapeutic use and side-effects.
If there is mutation data curated in GtoPdb this is indicated, with a link back to the appropriate section on the target detailed view page
Immuno ligand interactions - If available, a table of immuno-relevant ligands is shown. These ligands have been curated as having an association to the disease and possess interaction data with the target in GtoPdb. The approval status of the ligand is shown, along with curator comments and an indication of whether the target is considered the primary target of the ligand.
More information can be found in the help pages.
✖Kv1.3 | |
Role: | Associated with Multiple-Sclerosis, Type -1 Diabetes, Rheumatoid Arthritis and Psoriasis. Kv1.3 expression is increased in activated CCR7-effector memory T-cells. Blockers of this channel potently inhibit proliferation and cytokine secretion of effector memory T cells and have little or no effect on naive and central memory T-cells. |
Drugs: | Kaliotoxin treats experimental autoimmune encephalomyelitis (EAE) and bone resorption in experimental periodontal disease in rats. PAP-1 prevents experimental autoimmune diabetes and will suppress allergic contact dermatitis in rats. margatoxin suppresses delayed-type hypersensitivity in pigs. |
Side effects: | Inhibition of effector memory T-cells could potentially lead to reactivation of viral infections such as CMV. |
Therapeutic use: | ShK derivative and PAP-1 are in clinical development |
Comments: | Kv1.3 blockers are potentially useful for treating autoimmune diseases where terminally differentiated effector memory T cells are involved in pathogenesis. |
References: | 1-6 |
Click ligand name to view ligand summary page
Click the arrow in the final column to expand comments
More information can be found in the help pages.
✖No ligand related data available for Autoimmune disease
1. Beeton C, Barbaria J, Giraud P, Devaux J, Benoliel AM, Gola M, Sabatier JM, Bernard D, Crest M, Béraud E. (2001) Selective blocking of voltage-gated K+ channels improves experimental autoimmune encephalomyelitis and inhibits T cell activation. J Immunol, 166 (2): 936-44. [PMID:11145670]
2. Beeton C, Wulff H, Barbaria J, Clot-Faybesse O, Pennington M, Bernard D, Cahalan MD, Chandy KG, Béraud E. (2001) Selective blockade of T lymphocyte K(+) channels ameliorates experimental autoimmune encephalomyelitis, a model for multiple sclerosis. Proc Natl Acad Sci USA, 98 (24): 13942-7. [PMID:11717451]
3. Beeton C, Wulff H, Standifer NE, Azam P, Mullen KM, Pennington MW, Kolski-Andreaco A, Wei E, Grino A, Counts DR, Wang PH, LeeHealey CJ, S Andrews B, Sankaranarayanan A, Homerick D, Roeck WW, Tehranzadeh J, Stanhope KL, Zimin P, Havel PJ, Griffey S, Knaus HG, Nepom GT, Gutman GA, Calabresi PA, Chandy KG. (2006) Kv1.3 channels are a therapeutic target for T cell-mediated autoimmune diseases. Proc Natl Acad Sci USA, 103 (46): 17414-9. [PMID:17088564]
4. Koo GC, Blake JT, Talento A, Nguyen M, Lin S, Sirotina A, Shah K, Mulvany K, Hora Jr D, Cunningham P et al.. (1997) Blockade of the voltage-gated potassium channel Kv1.3 inhibits immune responses in vivo. J Immunol, 158 (11): 5120-8. [PMID:9164927]
5. Valverde P, Kawai T, Taubman MA. (2004) Selective blockade of voltage-gated potassium channels reduces inflammatory bone resorption in experimental periodontal disease. J Bone Miner Res, 19 (1): 155-64. [PMID:14753747]
6. Wulff H, Calabresi PA, Allie R, Yun S, Pennington M, Beeton C, Chandy KG. (2003) The voltage-gated Kv1.3 K(+) channel in effector memory T cells as new target for MS. J Clin Invest, 111 (11): 1703-13. [PMID:12782673]