Researchers ID Biomarker That Could Improve Autoimmune Disease Treatment
New research from the VA Portland Health Care System and Oregon Health & Sciences University has identified a biomarker that can potentially improve autoimmune disease treatment outcomes. The research team investigated ankylosing spondylitis (AS), an inflammatory disease that causes vertebrae in the spine to fuse together over time, to understand the condition’s underlying molecular mechanisms.
Also called axial spondyloarthritis, AS is a rare condition estimated to affect around 0.1-4.7% of the global population. It causes symptoms such as stooped posture, back pain, anemia, digestive illness, fatigue and weight loss. Scientists still don’t know the exact cause of the condition but theorize that the gene HLA-B27 significantly increases one’s risk of developing ankylosing spondylitis.
Ruth Napier, PhD and VA Portland principal investigator, senior researcher and assistant professor of molecular microbiology and immunology, arthritis and rheumatic disease at the OHSU School of Medicine, says the team’s research represents the first comprehensive efforts to determine how genetic markers can be used to improve ankylosing spondylitis treatment.
The team’s findings showed that using genetic markers to determine the most appropriate treatment for AS patients may have a positive impact on overall treatment. Napier said the findings put her and her team on the cusp of making a difference in AS treatments.
Although the condition is quite rare, affecting only 1 in 200 people, its symptoms are often severe and chronic, and can result in a significant reduction in quality of life. Furthermore, AS patients often suffer from autoimmune conditions such as psoriasis, inflammatory bowel disease and eye inflammation.
Treatment typically involves over-the-counter painkillers such as ibuprofen or naproxen followed by corticosteroid injections and even joint replacement surgery as the condition progresses.
AS patients also have the option of taking AS biotics, a class of protein-based and lab-made treatments that can stop inflammation by inhibiting proteins such as interleukin-17 (IL-17). Biologics target specific proteins but are effective only 40% of the time because physicians often struggle to decide which protein to target via biologics.
Prior research has found that slightly more 72% of AS proteins have a mutation in the CARD9 gene. This gene plays a significant role in the creation of proteins involved in immune response but is thought to go into overdrive thanks to mutations, causing immune cells such as neutrophils to go haywire and begin attacking healthy tissue.
After isolating and removing the CARD9 gene from mice, Napier’s team discovered that the mice without the gene did not develop AS. Further analysis of blood samples from hundreds of patients revealed that those with mutated CADR9 had significantly higher IL-17 protein concentrations in their blood compared to those with nonmutated genes. Consequently, Napier and her colleagues surmised that AS patients with mutated CAR9 genes can respond better to IL-17 inhibitor biologics, opening the door to more personalized treatments in the future.
As these researchers work to identify ways to block certain proteins that trigger autoimmune diseases such as AS, others at enterprises such as Scinai Immunotherapeutics Ltd. (NASDAQ: SCNI) are focusing on developing immunotherapies that can down-regulate the response of the immune system so that it stops attacking body tissues that are harmless.
NOTE TO INVESTORS: The latest news and updates relating to Scinai Immunotherapeutics Ltd. (NASDAQ: SCNI) are available in the company’s newsroom at https://ibn.fm/SCNI
Please see full terms of use and disclaimers on the BioMedWire website applicable to all content provided by BMW, wherever published or re-published: http://BMW.fm/Disclaimer
New research from the VA Portland Health Care System and Oregon Health & Sciences University has identified a biomarker that can potentially improve autoimmune disease treatment outcomes. The research team investigated ankylosing spondylitis (AS), an inflammatory disease that causes vertebrae in the spine to fuse together over time, to understand the condition’s underlying molecular mechanisms.
Also called axial spondyloarthritis, AS is a rare condition estimated to affect around 0.1-4.7% of the global population. It causes symptoms such as stooped posture, back pain, anemia, digestive illness, fatigue and weight loss. Scientists still don’t know the exact cause of the condition but theorize that the gene HLA-B27 significantly increases one’s risk of developing ankylosing spondylitis.
Ruth Napier, PhD and VA Portland principal investigator, senior researcher and assistant professor of molecular microbiology and immunology, arthritis and rheumatic disease at the OHSU School of Medicine, says the team’s research represents the first comprehensive efforts to determine how genetic markers can be used to improve ankylosing spondylitis treatment.
The team’s findings showed that using genetic markers to determine the most appropriate treatment for AS patients may have a positive impact on overall treatment. Napier said the findings put her and her team on the cusp of making a difference in AS treatments.
Although the condition is quite rare, affecting only 1 in 200 people, its symptoms are often severe and chronic, and can result in a significant reduction in quality of life. Furthermore, AS patients often suffer from autoimmune conditions such as psoriasis, inflammatory bowel disease and eye inflammation.
Treatment typically involves over-the-counter painkillers such as ibuprofen or naproxen followed by corticosteroid injections and even joint replacement surgery as the condition progresses.
AS patients also have the option of taking AS biotics, a class of protein-based and lab-made treatments that can stop inflammation by inhibiting proteins such as interleukin-17 (IL-17). Biologics target specific proteins but are effective only 40% of the time because physicians often struggle to decide which protein to target via biologics.
Prior research has found that slightly more 72% of AS proteins have a mutation in the CARD9 gene. This gene plays a significant role in the creation of proteins involved in immune response but is thought to go into overdrive thanks to mutations, causing immune cells such as neutrophils to go haywire and begin attacking healthy tissue.
After isolating and removing the CARD9 gene from mice, Napier’s team discovered that the mice without the gene did not develop AS. Further analysis of blood samples from hundreds of patients revealed that those with mutated CADR9 had significantly higher IL-17 protein concentrations in their blood compared to those with nonmutated genes. Consequently, Napier and her colleagues surmised that AS patients with mutated CAR9 genes can respond better to IL-17 inhibitor biologics, opening the door to more personalized treatments in the future.
As these researchers work to identify ways to block certain proteins that trigger autoimmune diseases such as AS, others at enterprises such as Scinai Immunotherapeutics Ltd. (NASDAQ: SCNI) are focusing on developing immunotherapies that can down-regulate the response of the immune system so that it stops attacking body tissues that are harmless.
NOTE TO INVESTORS: The latest news and updates relating to Scinai Immunotherapeutics Ltd. (NASDAQ: SCNI) are available in the company’s newsroom at https://ibn.fm/SCNI
Please see full terms of use and disclaimers on the BioMedWire website applicable to all content provided by BMW, wherever published or re-published: http://BMW.fm/Disclaimer
