MODULATING THE KV1.1 VOLTAGE-GATED POTASSIUM CHANNEL IN T-CELLS FOR REGULATING THE SYNTHESIS AND SECRETION OF TUMOR NECROSIS FACTOR (TNF- ) AND TREATING HUMAN DISEASES OR INJURIES MEDIATED BY DETRIMENTALLY HIGH OR LOW LEVELS OF TNF-

摘要

Blocking the voltage-gated potassium channel Kv1.1 of T-cells causes the robust and exclusive production of TNF-alpha, and thus can be used for eradication of cancer, improved eradication of infectious organisms, increased permeability of blood vessels and the blood brain barriers to given molecules and cells, and improved neuronal features, regeneration function and development. Blocking the voltage-gated potassium channel Kv1.1 of T-cells causes the robust and exclusive production of TNF-alpha. Similarly, unblocking of a blocked Kv1.1 channel or opening of a Kv1.1 channel will prevent the T-cells from producing and secreting excess amounts of TNF-alpha, thus being useful in the treatment of conditions such as rheumatoid arthritis and for treating neurological diseases associated with defected functioning and/or pathological block of the Kv1.1 channel, among them PNH associated with Kv1 Abs; Encephalitis associated with Kv1 Abs; and Episodic-ataxia type 1 (EA-1), in all of which the T-cell blocked Kv1.1 channel may secrete excess TNFa and thereby contribute to the pathology. Blocking of the Kv1.1 channel may be achieved in vivo or ex vivo by contact with a selective Kv1.1 channel blocking molecule such as Dendrotoxin-K or a selective monoclonal antibody against the Kv1.1 channel. Preventing the Kv1.1. block would be achieved by Kv1.1 openers, or by molecules that would prevent the closure of the Kv1.1 channel.