T-Cell Research
Posted: Wed Jun 15, 2005 7:14 am
Interesting research on T-cells that they tie into their drug under investigation (phase II), Neurovax.
The Immune Response Corporation and Oregon Health & Science University Collaboration Identifies FOXP3 as the Gene Marker for Impaired Immune Regulation in Multiple Sclerosis
Results May Lead To a New Therapeutic Approach to Treating MS
June 14, 2005 -- The Immune Response Corporation, a biopharmaceutical company dedicated to becoming a leading immune-based therapy company in HIV and multiple sclerosis (MS), announced today that clinical research conducted by the Company in association with Oregon Health & Science University (OHSU) has indicated that FOXP3, a specific genetic marker on T-cells known to be involved in maintaining immune tolerance and regulation of autoimmune diseases, is significantly reduced in patients with MS compared to healthy controls. These findings, published in the July issue of the Journal of Neuroscience Research, are significant to the Company because this deficiency of FOXP3 in MS patients is likely linked to deficient numbers of regulatory T-cells (also known as Treg cells). The Company believes that induction of these Treg cells is important to the mechanism of action for NeuroVax™, the Company’s peptide immune-based therapy.
Autoimmune diseases such as MS may result from the failure of tolerance mechanisms to prevent expansion of pathogenic T-cells. This paper establishes that MS patients have abnormalities in FOXP3 message and protein expression levels in peripheral Treg cells. This observation is the first to link a defect in functional peripheral immunoregulation to an established genetic marker, FOXP3, previously shown to be involved in maintaining immune tolerance and preventing development of autoimmune diseases. Diminished FOXP3 levels indicate impaired immunoregulation by Treg cells that may contribute to MS.
“Our research has demonstrated for the first time that MS patients have abnormalities in FOXP3 expression levels. This exciting discovery may allow us to track these cells and determine if immune-based therapies like NeuroVax™ can increase the level of Treg cells needed to inhibit inflammation caused by myelin-reactive T-cells thought to cause or worsen MS,” said Arthur A. Vandenbark, Ph.D., Senior Research Career Scientist at the VA Medical Center, and Professor of Neurology and Molecular Microbiology and Immunology at Oregon Health & Science University in Portland, Ore., and lead immunologist for this study. “We are continuing our ongoing clinical trials with NeuroVax™ and hope that these new findings will help better identify its therapeutic mechanism-of-action.”
“Preliminary data obtained in collaborative studies with OHSU indicate that NeuroVax™ may indeed induce increased levels of FOXP3 leading to increased production of specific Treg cells which would, in theory, control MS symptoms,” said Richard Bartholomew, Ph.D., Executive Director of Research and Development of The Immune Response Corporation. “This important research provides more information about NeuroVax™’s mechanism-of-action and builds upon our earlier studies. It is our strong belief that immune-based therapies, like NeuroVax™, can fill a need for safe and effective MS treatments.”
The published data was part of a clinical study conducted at OHSU under the Company’s FDA-registered investigational new drug (IND) application, and was partially funded by a grant from The Immune Tolerance Network. Blood was obtained from 19 healthy volunteer donors and 19 volunteer MS patients who were enrolled to begin participation in an ongoing open-label clinical trial with NeuroVax™. T-cell subpopulations were analyzed for FOXP3 expression by using realtime polymerase chain reaction (PCR) to quantitate FOXP3 message and by Western blots to quantitate FOXP3 protein expression.
http://www.imnr.com/news/2005/2005JUN14.htm
The Immune Response Corporation and Oregon Health & Science University Collaboration Identifies FOXP3 as the Gene Marker for Impaired Immune Regulation in Multiple Sclerosis
Results May Lead To a New Therapeutic Approach to Treating MS
June 14, 2005 -- The Immune Response Corporation, a biopharmaceutical company dedicated to becoming a leading immune-based therapy company in HIV and multiple sclerosis (MS), announced today that clinical research conducted by the Company in association with Oregon Health & Science University (OHSU) has indicated that FOXP3, a specific genetic marker on T-cells known to be involved in maintaining immune tolerance and regulation of autoimmune diseases, is significantly reduced in patients with MS compared to healthy controls. These findings, published in the July issue of the Journal of Neuroscience Research, are significant to the Company because this deficiency of FOXP3 in MS patients is likely linked to deficient numbers of regulatory T-cells (also known as Treg cells). The Company believes that induction of these Treg cells is important to the mechanism of action for NeuroVax™, the Company’s peptide immune-based therapy.
Autoimmune diseases such as MS may result from the failure of tolerance mechanisms to prevent expansion of pathogenic T-cells. This paper establishes that MS patients have abnormalities in FOXP3 message and protein expression levels in peripheral Treg cells. This observation is the first to link a defect in functional peripheral immunoregulation to an established genetic marker, FOXP3, previously shown to be involved in maintaining immune tolerance and preventing development of autoimmune diseases. Diminished FOXP3 levels indicate impaired immunoregulation by Treg cells that may contribute to MS.
“Our research has demonstrated for the first time that MS patients have abnormalities in FOXP3 expression levels. This exciting discovery may allow us to track these cells and determine if immune-based therapies like NeuroVax™ can increase the level of Treg cells needed to inhibit inflammation caused by myelin-reactive T-cells thought to cause or worsen MS,” said Arthur A. Vandenbark, Ph.D., Senior Research Career Scientist at the VA Medical Center, and Professor of Neurology and Molecular Microbiology and Immunology at Oregon Health & Science University in Portland, Ore., and lead immunologist for this study. “We are continuing our ongoing clinical trials with NeuroVax™ and hope that these new findings will help better identify its therapeutic mechanism-of-action.”
“Preliminary data obtained in collaborative studies with OHSU indicate that NeuroVax™ may indeed induce increased levels of FOXP3 leading to increased production of specific Treg cells which would, in theory, control MS symptoms,” said Richard Bartholomew, Ph.D., Executive Director of Research and Development of The Immune Response Corporation. “This important research provides more information about NeuroVax™’s mechanism-of-action and builds upon our earlier studies. It is our strong belief that immune-based therapies, like NeuroVax™, can fill a need for safe and effective MS treatments.”
The published data was part of a clinical study conducted at OHSU under the Company’s FDA-registered investigational new drug (IND) application, and was partially funded by a grant from The Immune Tolerance Network. Blood was obtained from 19 healthy volunteer donors and 19 volunteer MS patients who were enrolled to begin participation in an ongoing open-label clinical trial with NeuroVax™. T-cell subpopulations were analyzed for FOXP3 expression by using realtime polymerase chain reaction (PCR) to quantitate FOXP3 message and by Western blots to quantitate FOXP3 protein expression.
http://www.imnr.com/news/2005/2005JUN14.htm