Latest news with #autoimmuneDiseases
Wall Street Journal
09-07-2025
- Business
- Wall Street Journal
Vie Ventures Launches to Bankroll Autoimmune-Disease Biotechs
Two veteran life-sciences investors have launched Vie Ventures, which plans to fund biotechnology startups targeting autoimmune diseases and connect them with nonprofits that might accelerate their drug development. Vie Co-founders Luke Evnin and Dr. Steven St. Peter previously invested together with MPM Capital, now MPM BioImpact. Both also have experience with nonprofits: Evnin is chairman of the Scleroderma Research Foundation and St. Peter most recently was managing director of the T1D Fund, the venture-philanthropy arm of Breakthrough T1D, which supports Type 1 diabetes research.
Medical News Today
09-07-2025
- Health
- Medical News Today
Clinical test may predict best rheumatoid arthritis biologic for each individual
Rheumatoid arthritis is a painful, progressive joint disease characterized by particularly acute used to treat autoimmune diseases such as rheumatoid arthritis, target symptom mechanisms without compromising the entire immune system.A new test may take the guesswork out of finding the right biological therapy for people with rheumatoid at Queen Mary, University of London, have announced a new machine-learning-based method for predicting the biological therapy, or biologic, most likely to successfully relieve symptoms for an individual with rheumatoid scientists say that their system successfully predicted the optimal biologic for 79–85% of patients on its first try in validation the last 20 years, biologics have revolutionized the treatment of rheumatoid arthritis (RA) due to their potential to focus on the underlying cellular cause of a patient's RA is an immune disorder, conventional treatments suppress the function of the entire immune system to reduce symptoms of the condition. Absent a robust immune system, the patient is left vulnerable to idea behind biologics is that a more precise approach can be effective at reducing RA symptoms without significantly compromising the immune to its inventors, prior to the newly announced technique, identifying the correct biologic for each patient was somewhat of a hit-or-miss procedure — 40% of biological therapies fail due to inaccurate new prediction technique pinpoints which of the three main types of biologics shows the most promise for a patient.'This innovation could have major benefits for patients and healthcare providers alike. Prescribing the right treatment the first time would reduce patient suffering,' Professor Constantino Pitzalis, study author, tells Medical News scientists announced their new method of identifying the best biologic for an individual RA patient in Nature rheumatoid arthritis is treatedRheumatoid arthritis is an autoimmune disease that causes pain and inflammation in and around the joints.'The persistent inflammation can impair mobility and dexterity, making daily tasks difficult or impossible,' explained Syeda S. Nasrin, MSc, graduate of the Center for Regenerative Sciences in Dresden, Germany, who was not involved in the Bowen, PhD, bioethicist at SUNY Upstate Medical University, who was also not involved in the study, is someone who has personal experience with RA. 'When I developed RA, the pain was shocking. I'd wake up in tears in the middle of the night and no amount of NSAIDs, ice, heat, movement, rest — any of the usual things you'd try for joint pain — even began to offer relief. It spreads all over the body and makes basic life tasks, like putting on a shirt or opening a car door, agonizing,' she is a chronic and progressive condition, and may also involve other parts of the from biologics, people with RA may be treated with immune suppressors such as methotrexate and Janus kinase (JAK) inhibitors, which target the overactive immune system. For pain, doctors prescribe NSAIDs, which are notoriously hard on the stomach and GI tract with long-term use, and corticosteroids to control do biological therapies work?'Biologics,' said Nasrin, 'target specific cellular pathways in the immune system that play key roles in the inflammatory process of RA.'The idea is to address the mechanism causing an individual patient's RA-related joint inflammation without attacking the immune system itself.'For instance,' she explained, 'Interleukin-6 (IL-6) is a cytokine that is involved in immune cell modulation and inflammation. Tocilizumab (Actemra), a monoclonal antibody, can inhibit this IL-6 cytokine and reduce inflammation.'Nasrin made clear, however, that 'as far as I know, these molecular targeted therapies are able to reduce inflammation, slow joint damage, and improve physical function, but they do not cure the disease.'Why getting the right biologic is importantSince it currently takes time to identify a biologic that can address a specific patient's RA, there is an extended period during which no symptom relief are also risks associated with this period of experimentation, pointed out Nasrin. 'As these approaches often include altering the immune system at a molecular level, that means there is a suppression of the immune system in the body. This could increase infection susceptibility.'Bowen pointed out as well that even the right biologic takes time to have a positive effect on symptoms. Extended periods of trial and error may be accompanied by uncertainty in addition to the ongoing physical Bowen described it, 'What works for one person may not work for another. So it can be really demoralizing and isolating if, say, you're looking around and seeing all these people who are doing great on [one biologic], but it's doing nothing for you.''It's grueling,' she said, 'not just on a physical level but also a psychological one, where you might be dealing with huge amounts of fear, hopelessness, and doubt that you will ever find something that works.'Predicting the best drug for each individualThe new method identifies which of three biologics — etanercept, tocilizumab, or rituximab — is most likely to work for a a recent clinical trial that involved deep molecular phenotyping, the scientists developed a database of gene differences in RA patients who had responded well to biologics, compared to others who did were also able to ascertain the response of specific groups of RA-related cells to each of the drugs. From there, they built three predictive models for the three biologics to test how well a patient would do with a given predict the correct biologic for a specific patient, they extract a tissue sample from a joint affected by RA, and score the levels of activity in 524 genes they have identified as relevant. They can then match those scores to the most promising Mary, University of London, is seeking commercial partners to help develop the predictive system for real-world use. No timetable for when this may occur has yet been the validation results are promising, Nasrin, struck a note of caution:'Personalized medicine is still at a very early stage of development. So the approach should be taken with caution and only proceed with having solid clinical trial data.'Clinical trials are reportedly underway.
Medscape
04-07-2025
- Health
- Medscape
Autoimmune Skin Diseases Tied to Better Cancer Survival
TOPLINE: Patients with autoimmune skin diseases (ASDs) showed significantly lower risks for death after cancer treatment than those without ASDs, especially those with alopecia areata or Sjögren syndrome. METHODOLOGY: A population-based cohort study analyzed data from Taiwan's Nationwide Cancer Registry and National Health Insurance Database between January 2019 and June 2021. Researchers evaluated 197,895 adults, including 26,008 with ASD (mean age, 64 years; 57.6% women) and 171,887 who did not have an ASD (mean age, 62.8 years; 46.9% women), who received antineoplastic treatment, including chemotherapy, targeted therapy, or immunotherapy. Primary outcomes were all-cause mortality and cancer-specific mortality. The mean follow-up was 566.7 days. TAKEAWAY: Patients with ASDs showed a significantly lower risk for all-cause mortality (adjusted hazard ratio [aHR], 0.93; P < .001) and cancer-specific mortality (aHR, 0.93; P < .001) than those without ASDs, adjusted for factors including age, sex, and prior immunosuppressive drug use. Alopecia areata showed the strongest association with reduced all-cause mortality risk (aHR, 0.82; P < .001), followed by Sjögren syndrome (aHR, 0.87; P < .001), vitiligo (aHR, 0.89; P < .05), and lupus erythema (aHR, 0.90; P < .05). Similarly, patients with alopecia areata showed the highest inverse associations with cancer-specific mortality (aHR, 0.82; P < .001), followed by those with Sjögren syndrome (aHR, 0.88; P < .001), vitiligo (aHR, 0.88; P < .05), and lupus erythema (aHR, 0.81; P < .001). The associations remained consistent after adjusting for potential confounders and across most cancer types, stages, and treatment regimens. IN PRACTICE: 'This population-based cohort study demonstrated that patients with ASDs, particularly alopecia areata and Sjögren syndrome, experienced better survival outcomes, indicating that ASDs play an important role in cancer prognosis,' the study authors wrote. 'Future studies are necessary to better understand the underlying immune mechanisms and explore how this knowledge can be applied to enhance patient care,' they added. SOURCE: The study was led by Li-Ting Kao, PhD, School of Pharmacy, National Defense Medical Center in Taipei, Taiwan, and was published online on July 2 in JAMA Dermatology. LIMITATIONS: The study did not account for potential confounding factors such as lifestyle factors, genetic predisposition, and environmental exposures. Additionally, clinical data on ASD severity, such as the extent of skin lesions, were unavailable. DISCLOSURES: The study received support through grants from the Ministry of Science and Technology, Taiwan. Kao disclosed receiving grants from IQVIA outside the submitted work. This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
Yahoo
25-06-2025
- Health
- Yahoo
Mitochondria can sense bacteria and trigger your immune system to trap them – revealing new ways to treat infections and autoimmunity
Mitochondria have primarily been known as the energy-producing components of cells. But scientists are increasingly discovering that these small organelles do much more than just power cells. They are also involved in immune functions such as controlling inflammation, regulating cell death and responding to infections. Research from my colleagues and I revealed that mitochondria play another key role in your immune response: sensing bacterial activity and helping neutrophils, a type of white blood cell, trap and kill them. For the past 16 years, my research has focused on understanding the decisions immune cells make during infection and how the breakdown of these decision-making processes cause disease. My lab's recent findings shed light on why people with autoimmune diseases such as lupus may struggle to fight infections, revealing a potential link between dysfunctional mitochondria and weakened immune defenses. Neutrophils are the most abundant type of immune cell and serve as the immune system's first responders. One of their key defense mechanisms is releasing neutrophil extracellular traps, or NETs – weblike structures composed of DNA and antimicrobial proteins. These sticky NETs trap and neutralize invading microbes, preventing their spread in the body. Until recently, scientists believed that NET formation was primarily triggered by cellular stress and damage. However, our study found that mitochondria can detect a specific bacterial byproduct – lactate – and use that signal to initiate NET formation. Lactate is commonly associated with muscle fatigue in people. But in the context of bacterial infections, it plays a different role. Many bacteria release lactate as part of their own energy production. My team found that once bacteria are engulfed by a compartment of the cell called the phagosome, neutrophils can sense the presence of this lactate. Inside the phagosome, this lactate communicates to the neutrophil that bacteria are present and that the antibacterial processes are not sufficient to kill these pathogens. When the mitochondria in neutrophil cells detect this lactate, they start signaling for the cell to get rid of the NETs that have entrapped bacteria. Once the bacteria are released outside the cell, other immune cells can kill them. When we blocked the mitochondria's ability to sense lactate, neutrophils failed to produce NETs effectively. This meant bacteria were more likely to escape capture and proliferate, showing how crucial this mechanism is to immune defense. This process highlights an intricate dialogue between the bacteria's metabolism and the host cell's energy machinery. What makes this finding surprising is that the mitochondria within cells are able to detect bacteria trapped in phagosomes, even though the microbes are enclosed in a separate space. Somehow, mitochondrial sensors can pick up cues from within these compartments – an impressive feat of cellular coordination. Our study is part of a growing field called immunometabolism, which explores how metabolism and immune function are deeply intertwined. Rather than viewing cellular metabolism as strictly a means to generate energy, researchers are now recognizing it as a central driver of immune decisions. Mitochondria sit at the heart of this interaction. Their ability to sense, respond to and even shape the metabolic environment of a cell gives them a critical role in determining how and when immune responses are deployed. For example, our findings provide a key reason why patients with a chronic autoimmune disease called systemic lupus erythematosus often suffer from recurrent infections. Mitochondria in the neutrophils of lupus patients fail to sense bacterial lactate properly. As a result, NET production was significantly reduced. This mitochondrial dysfunction could explain why lupus patients are more vulnerable to bacterial infections – even though their immune systems are constantly activated due to the disease. This observation points to mitochondria's central role in balancing immune responses. It connects two seemingly unrelated issues: immune overactivity, as seen in lupus, and immune weakness like increased susceptibility to infection. When mitochondria work correctly, they help neutrophils mount an effective, targeted attack on bacteria. But when mitochondria are impaired, this system breaks down. Our discovery that mitochondria can sense bacterial lactate to trigger NET formation opens up new possibilities for treating infections. For instance, drugs that enhance mitochondrial sensing could boost NET production in people with weakened immune systems. On the flip side, for conditions where NETs contribute to tissue damage – such as in severe COVID-19 or autoimmune diseases – it might be beneficial to limit this response. Additionally, our study raises the question of whether other immune cells use similar mechanisms to sense microbial metabolites, and whether other bacterial byproducts might serve as immune signals. Understanding these pathways in more detail could lead to new treatments that modulate immune responses more precisely, reducing collateral damage while preserving antimicrobial defenses. Mitochondria are not just the powerhouses of the cell – they are the immune system's watchtowers, alert to even the faintest metabolic signals of bacterial invaders. As researchers' understanding of their roles expands, so too does our appreciation for the complexity – and adaptability – of our cellular defenses. This article is republished from The Conversation, a nonprofit, independent news organization bringing you facts and trustworthy analysis to help you make sense of our complex world. It was written by: Andrew Monteith, University of Tennessee Read more: Mitochondria keep your brain cells alive − helping them run smoothly may protect against Parkinson's disease More than half of US teens have had at least one cavity, but fluoride programs in schools help prevent them – new research When COVID-19 or flu viruses kill, they often have an accomplice – bacterial infections Andrew Monteith receives funding from the National Institute of Health.
Associated Press
23-06-2025
- Business
- Associated Press
Harbour BioMed Enters Global Strategic Collaboration with Otsuka to Advance BCMAxCD3 Bispecific T-Cell Engagers
CAMBRIDGE, Mass., ROTTERDAM, Netherlands and SHANGHAI, June 22, 2025 /PRNewswire/ -- Harbour BioMed (HKEX: 02142), a global biopharmaceutical company committed to the discovery and development of novel antibody therapeutics in immunology and oncology, today announced a global strategic collaboration with Otsuka Pharmaceutical Co., Ltd. ('Otsuka') to advance BCMAxCD3 bispecific T-cell engagers for the treatment of autoimmune diseases. Under the terms of the agreement, Otsuka is granted an exclusive license to develop, manufacture, and commercialize HBM7020, a BCMAxCD3 bispecific T-cell engager globally, excluding Greater China (Mainland China, Hong Kong, Macau and Taiwan). In return, Harbour BioMed will receive a total of $47 million in upfront and near-term payments. The company is also eligible for additional payments of up to $623 million upon the achievement of specified development and commercial milestones, as well as tiered royalties on future net sales. This strategic collaboration establishes a foundation for potential future partnerships between the two companies in the T-cell engager area. 'We are delighted to collaborate with Otsuka, a global healthcare leader renowned for its innovative approach to addressing unmet medical needs,' said Dr. Jingsong Wang, Founder, Chairman, and CEO of Harbour BioMed. 'This collaboration underscores the strength of Harbour BioMed's proprietary Harbour Mice® and HBICE® technology platforms, which enable the rapid development of fully human bispecific antibodies with optimized safety and efficacy profiles. By leveraging our unique capabilities, we are well-positioned to advance next-generation biotherapeutics that can make a meaningful difference in patients' lives worldwide.' Makoto Inoue, President and Representative Director of Otsuka Pharmaceutical, noted, 'Otsuka is expanding our development pipeline in the autoimmune disease field by leveraging the antibody drug platform of our subsidiary Visterra, and the small molecule drug discovery platform of our subsidiary Jnana. HBM7020 is expected to demonstrate efficacy in a broad range of autoimmune diseases in which B cells play a major role in disease pathogenesis, and we hope to contribute further to the field of specialized autoimmune diseases and thereby benefit patients.' About HBM7020 HBM7020 is a BCMAxCD3 bispecific antibody generated using Harbour BioMed's fully human HBICE® bispecific technology and Harbour Mice® platform. It is designed to crosslink target cells and T cells by binding to BCMA and CD3 on the cell surface, leading to potent T cell activation and targeted cell elimination. By incorporating dual anti-BCMA binding sites for enhanced cell targeting and monovalent-optimized CD3 activity to minimize cytokine release syndrome (CRS), HBM7020 has demonstrated potent cytotoxicity with broad therapeutic potential in both immunological and oncological diseases. In August 2023, HBM7020 obtained IND clearance from the National Medical Products Administration (NMPA) to commence a Phase I trial for cancer in China. About Harbour BioMed Harbour BioMed (HKEX: 02142) is a global biopharmaceutical company committed to the discovery and development of novel antibody therapeutics in immunology and oncology. The company is building a robust and differentiated pipeline through internal R&D capabilities, strategic global collaborations in co-discovery and co-development, and selective acquisitions. Harbour BioMed's proprietary antibody technology platform, Harbour Mice®, generates fully human monoclonal antibodies in both the conventional two heavy and two light chain (H2L2) format and the heavy chain-only (HCAb) format. Building upon HCAb antibodies, the HCAb-based immune cell engagers (HBICE®) bispecific antibody technology enables tumor-killing effects that traditional combination therapies cannot achieve. Additionally, the HCAb-based bispecific immune cell antagonist (HBICATM) technology empowers the development of innovative biologics for immunological and inflammatory diseases. By integrating Harbour Mice®, HBICE®, and HBICATM with a single B-cell cloning platform, Harbour BioMed has built a highly efficient and distinctive antibody discovery engine for developing next-generation therapeutic antibodies. For more information, please visit . About Otsuka Pharmaceutical Co., Ltd. Otsuka Pharmaceutical Co., Ltd. is a total healthcare company that focuses on each individual's potential to enhance their well-being. Our medical-related business provides treatments and diagnostics for both physical and mental health. Our nutraceutical business supports daily health maintenance and improvement. Otsuka's unique products and services are based on scientific evidence, under the guidance of our corporate philosophy: Otsuka-people creating new products for better health worldwide. For further information, please visit View original content to download multimedia: SOURCE Harbour BioMed
