News
Nichols, Muthukrishnan Earn $2.4M R01 Grant for Center for Musculoskeletal Research - Will Explore Gamma Delta T Cells’ Role in Tendon Adhesion Formation
Thursday, October 29, 2026
Anne E.C. Nichols, PhD, and Gowri Muthukrishnan, PhD, researchers at the Center for Musculoskeletal Research at the University of Rochester, have earned a $2.4M R01 grant to study the causes and potential treatments for adhesion formation in tendon, the leading cause of impaired recovery after tendon surgery. Nichols, Muthukrishnan and their labs will study a previously unexplored interaction between T cells and tendon-resident cells and examine whether disrupting IL-17 signaling using existing FDA-approved IL-17-targeting biologics could be helpful in reducing adhesion formation and improve tendon healing.
A new treatment would be welcome news for the 300,000 people in the U.S. who have tendon repair surgeries every year. Flexor tendon injury in the hand is one of the most common types of tendon injury. Surgery to knit the two severed ends together is the leading treatment approach, but adhesive scar formation around the surgery site is a common complication, contributing to pain and loss of function. As many as 24 percent of patients with injured flexor tendons require a second surgery to remove excess scar tissue to restore tendon function.
Current therapeutic approaches fail to effectively prevent or reverse adhesion formation. There is little understanding of the cellular players or molecular drivers involved in post-injury tendon adhesion formation, but Nichols’s research has led to new discoveries, and she has multiple projects under way to investigate the dynamic molecular processes that occur after injury occurs and during healing.
An Intriguing New Suspect in Tendon Scar Formation: Epitenon Cells
Most earlier tendon studies focused on tenocytes, specialized cells found in tendons that produce and maintain the tendon's structure. In research published in Nature Communications in 2025, the Nichols lab was the first to trace and manipulate a key player in the healing process – the epitenon cells that form a thin outer layer surrounding the tendon – and show the remarkable similarity between these cells’ activity in mice and humans.
The team found that a portion of epitenon cells followed tenocytes into the crucial bridging tissue that helps tendons repair, but a larger percentage migrated to form a capsule of adhesive scar tissue around the injury site. When the Nichols lab killed epitenon-derived cells using a genetically encoded toxin, they confirmed that suppressing the cells at the right time and place in the healing trajectory significantly improved tendon range of motion in mice.
Their discovery raised the possibility for new translational treatments, but key questions remain.
“While the fate of the epitenon cells is increasingly well-defined, the upstream cues and cellular interactions that drive their adhesion-forming behavior post-injury remain poorly understood, limiting the development of targeted therapies to reduce adhesions and improve tendon healing,” said Nichols, assistant professor of Orthopaedics.
Another challenge: the tools used to kill epitenon cells in mouse models won’t translate to humans, “so we worked to identify an alternative pathway and cell population that might be interacting with epitenon cells and driving them to cause adhesions to form,” Nichols said. One of the prime targets was immune cells, given their known fibrosis-causing activities in other tissues.
“I knew I was looking for an immune cell that was communicating with epitenon cells through some pro-fibrotic pathway, but that was about it. When I brought the idea to my friend and colleague Gowri, he immediately thought it might be T cells based on his own work. Working together, we then identified a potential interaction between epitenon cells and gamma delta T cells through IL-17 signaling.”
A CMSR Advantage: Cross-Lab Collaboration That Fosters Discovery
The Nichols-Muthukrishnan project underscores one of CMSR’s signature strengths: collaboration between research labs with different areas of focus and competencies often leads to new opportunities for discovery, and an outcome greater than the sum of its parts. The Nichols lab focuses on the causes of tendon scar formation and potential treatment options; Muthukrishnan is an immunologist whose work explores how dysregulated immune responses shapes musculoskeletal diseases. By bridging their separate areas of expertise, they discovered commonalities in how cells behave in the presence of injury and chronic infection.
For this project, they will focus on gamma delta T cells, the most prevalent T cell type found in healing tendon and the only ones to produce interleukin-17A (IL-17A), a cytokine known to promote scar formation in other tissues. Epitenon cells also express the receptor for IL-17A, which indicates direct communication between these cell types after injury. Disrupting that communication could lead to a new treatment approach.
“We were really interested because in other fibrotic situations these T cells are known to push other resident cells to become pro-fibrotic,” said Muthukrishnan, associate professor of Orthopaedics, Microbiology and Immunology. “IL-17A signaling may be the key to blocking adhesion formation in tendon. And since there are FDA-approved drugs that target IL-17A drugs already in existence, this is a great avenue of exploration.”
“If we can show that these drugs that are already approved for separate conditions could work in our tendon injury model, that would be a quick pathway to clinical translation versus having to come up a brand-new drug. We’re excited to pursue this because immunology in tendon is still not a very well-developed field,” Nichols said.
Muthukrishnan agreed: “The exciting thing about this whole project is that some of the phenomena that Anne described in adhesion formation in her tendon injury model is similar to the work we do in my lab to understand how immune cells behave in the presence of a chronic infection. We were able to draw many parallels between her work and mine as we worked to design this collaborative research project.”
Project Goals
The project aims for the five-year grant project are:
- Study the spatial relationship and potential interactions between gamma delta T cells and epitenon cells during adhesion formation over time to identify when and where the cells’ behavior can be blocked to prevent adhesions.
- Investigate how the cell types interact to better understand the cellular and molecular mechanisms that lead to formation of tendon adhesions.
The researchers will evaluate the therapeutic potential of using an anti-IL-17 biologic to block adhesion formation.
CMSR Members Recognized at ASBMR 2026 Annual Meeting
Monday, October 26, 2026
The CMSR was strongly represented at the American Society for Bone and Mineral Research (ASBMR) 2026 Annual Meeting held in Boston, Massachusetts, on October 9-12, 2026. The ASBMR Annual Meeting is the world's largest meeting in the bone, mineral, and musculoskeletal research field. A number of CMSR attendees - faculty and students alike - received recognition at the event, reinforcing the CMSR's continued excellence in musculoskeletal research.
Below is a list of attendees and their recognitions.
- Dr. Laura Calvi - Fellow of ASBMR and Invited Speaker
- Dr. Sarah Catheline - Mid-Career Award and Plenary Poster
- Dr. Roman Eliseev - Mid-Career Award and Invited Speaker
- Dr. Chia-Lung Wu - Invited Speaker
- Ryan Adapathya (Yeh Lab) - President's Award
- Sandra Castillo Aguirre (Eliseev Lab) - Plenary Poster Award and Mentoring Award
- Renae Duncan (Eliseev Lab) - Plenary Poster Award and Travel Award
- Amy Hong (Yeh Lab) - Plenary Poster Award and Travel Award
- Kevin Lee (Yeh Lab) - Travel Award
- Yiwei Lu (H. Zhang Lab) - Young Investigator Award
- Eliya Tashbib (Wu Lab) - Young Investigator Award
Congratulations to all on their achievements!
Irwin Receives $599K from NIH National Institute on Aging for New Sponsored Research Project
Monday, August 24, 2026
Assistant Professor Rebecca Irwin from the Department of Biomedical Engineeringreceived $599,180 from the NIH National Institute on Aging for a project titled “Longitudinal Intravital Multiphoton Imaging of the Murine Intervertebral Disc to Reveal Age-Associated Mechanisms of Degeneration.”
Congratulations, Becka!
Tissue-on-a-Chip Tech Could Speed Cures from Clinical Trials
Tuesday, August 11, 2026
University of Rochester researchers Hani Awad, James McGrath, and Benjamin Miller are leading federally funded tissue-on-a-chip research projects on the River and Health Sciences campuses. The worldwide pursuit of tissue-on-a-chip devices that are reliable and robust enough to replicate human biology has been accelerated in the U.S. through federal mandates, along with grants to a handful of select academic research powerhouses including Duke, Harvard, Johns Hopkins, and the University of Rochester.
Tissue chips are bioengineered, microfluidic devices embedded with human cells in a way that keeps them alive for days or even weeks. They mimic physical, biological, and even mechanical environments of human tissue and organs so that scientists can observe cell interactions and responses when studying disease or testing potential cures. This could largely replace current testing for disease modeling, drug discovery, toxicology screening, and even personalized medicine. The hope is to improve on, and one day even replace, mouse experiments that have been the standard of scientific inquiry for the last 100 years. When perfected, the technology could limit animal testing as well as speed clinical trials and avoid the potential catastrophe of a human trial that causes unforeseen harm to participants.
(From left) Benjamin Miller,
Hani Awad, and James McGrath
Muthukrishnan Earns $2.7M NIH Grant to Study Immune Dysfunction in Bone Infection
Tuesday, June 23, 2026
Gowri Muthukrishnan, PhD, assistant professor in the departments of Orthopaedics and Microbiology and Immunology, has earned a $2.7 million grant from NIH to study potential diagnostic and treatment options for implant-associated bone infection.
They are one of the most serious complications in orthopaedic surgery, with Staphylococcus aureus the leading cause of persistent cases. Despite advances in surgery and antibiotic therapy, recurrent and persistent S. aureus infections remain a major challenge in orthopaedic care, and reinfection rates following orthopaedic surgery have changed little over the past several decades. There are no evidence-based clinical assessment tools to evaluate severity of bone infection that could aid clinicians in patient care. At the same time, some patients recover from asymptomatic cases on their own; Muthukrishnan and other researchers are interested in how their immune systems effectively fight the infection, as it may lead to potential new prophylactic approaches or treatments.
The NIH grant will support Muthukrishnan’s research to better understand the mechanics of implant-associated bone infection; seek a host immune biomarker that could aid clinicians predict disease severity and treatment outcomes; and explore whether drugs now used in cancer treatment could help fight bacterial bone infection.
In prior research aimed at developing clinical biomarkers, Muthukrishnan’s lab performed host studies in a humanized mouse model and found that implant-associated osteomyelitis is characterized by increases in bacterial load and bone osteolysis, along with large numbers of proliferating human T cells adjacent to purulent abscesses in the bone marrow. The high levels of immune checkpoint proteins in patients with prosthetic joint infections were particularly apparent in patients with poor outcomes, including amputation due to persistent infection and septic death.
The work confirmed that during bone infections, there is dysregulated immune function; T cells experience “exhaustion” due to constant antigenic stimulation from bacteria, which prevents them from performing their intended immune functions effectively. Muthukrishnan’s research showed that serum immune checkpoint protein levels could predict patient outcomes with 90 percent accuracy, which could help orthopedic surgeons determine whether patients should receive aggressive or conservative treatment for joint infections. A biomarker could signal the severity of infection and shed light on why some patients’ bodies fight the infection successfully while others suffer devastating complications, including arthrodesis, reinfection, amputation, and septic death.
As part of the project, Muthukrishnan will assess patients based on their T cell exhaustion profiles. The NIH award will support one of the first comprehensive investigations into T cell exhaustion as both a biomarker and therapeutic target in orthopaedic infection. Immune checkpoint pathways triggered in cancer are also activated in bone infections; the research will explore whether immune checkpoint blockade drugs approved for cancer treatment could mitigate the infection burden and reprogram exhausted T cells, restore antibacterial immunity, and improve infection control. There are more than 2600 ongoing clinical trials for the drugs, but very limited research to date on their use for bacterial infection.
As part of the project, Muthukrishnan will collaborate with orthopedic surgeons to collect bone marrow samples during revision surgeries to analyze T cell exhaustion phenotypes.
“We hypothesize that persistent S. aureus infections cause impairment of CD4+ Th1/Th17 cells and can be leveraged as a functional biomarker of S. aureus implant-associated osteomyelitis disease outcome,” Muthukrishnan said.
Ultimately, Muthukrishnan aims to develop a simple blood test to help determine whether patients should receive aggressive or conservative treatment, and whether the FDA-approved checkpoint blockade drugs could become a standard of care for bone infections.
NIH S10 Award Will Expand Advanced Imaging Capabilities Across URochester Medicine
Wednesday, June 17, 2026
Published in the Center for Advanced Research Techologies (CART) Newsletter
The University of Rochester has received an NIH Shared Instrumentation Grant (S10) to acquire a Bruker SkyScan 1276 CMOS Edition High-Resolution In Vivo MicroCT System, led by Hani Awad, PhD, Professor of Orthopaedics and member of the Center for Musculoskeletal Research. The approximately $466,000 award will support the purchase of a next-generation imaging platform that will be housed within the Biomechanics and Multimodal Tissue Imaging Core, replacing an aging scanner and significantly enhancing the institution’s capacity for high-resolution, longitudinal imaging studies. The system offers true spatial resolution down to 6 μm and advanced physiological monitoring capabilities, enabling researchers to visualize biological structures and disease processes with unprecedented detail.
The new microCT system will serve a broad community of NIH-funded investigators across University of Rochester Medicine, supporting research in musculoskeletal biology, cancer, cardiovascular disease, immunology, oral and craniofacial sciences, regenerative medicine, and other fields. Expected to support more than 1,600 hours of annual use, the instrument represents a significant investment in shared research infrastructure that will accelerate discovery, strengthen cross-disciplinary collaborations, and expand opportunities for translational research. This award reflects the collaborative spirit that drives scientific innovation at Rochester and highlights the impact of shared resources in advancing research across the institution.
TraCe-bMPS: Advancing Human Tissue-on-Chip Models for Discovery, Translation, and Drug Development
Wednesday, June 17, 2026
Published in the Center for Advanced Research Techologies (CART) Newsletter
The Translational Center for Barrier Microphysiological Systems (TraCe-bMPS) is a consortium of industry and academia that is developing and applying chip-based models of human tissue for both discovery and regulatory drug development. Based at the University of Rochester, TraCe-bMPS grew out of collaborations between bioengineering labs with complementary strengths in materials, bio-sensing, and disease modeling. These teams created uniquely capable technologies for building and measuring compartmentalized models of human tissue. In TraCe-bMPS, the technology development teams are joined by regulatory and pharmaceutical scientists who bring quality systems, SOP development, and the reproducibility standards needed for the chips to support clinical drug development programs.
TraCe-bMPS teams are using the center’s tissue-on-chip platforms to model a range of healthy and diseased tissues in a number of contexts. Current efforts include models of neurovascular injury, inflammatory arthritis, connective tissue repair, retinal barrier function, and innate immunity. Some tissue chips are developed in collaboration with pharmaceutical and academic partners with specific clinical and preclinical endpoints in mind. Others are used as platforms for discovery and hypothesis testing about the nature of multicellular interactions in disease origins and progression.
The adoption of human microphysiological systems and other non-animal methodologies (NAMS) is being driven by federal mandates and an ever-growing interest in the reduction of animal use in biomedical research and drug development. TraCe-bMPS is a new type of core facility that is appearing at universities to meet the need for rapid adoption of NAMS by biomedical research programs. TraCe-bMPS has packaged its core capabilities as services to help teams internal and external to Rochester adopt NAMS. The center operates a service core providing quality-controlled chip components, validated protocols, and technical support to investigators across universities, medical centers, and industry labs. To date, more than 20,000 devices have been built and used in research laboratories around the world. TraCe-bMPS also supports adoption through a training program at Rochester, and external workshops.
If interested in learning more, contact Jim McGrath or visit the website →
Calvin Cole, Zach Sechrist: Mentorship That Shapes the Whole Scientist
Tuesday, April 28, 2026
From the Faculty Focus Newsletter, Education Update
In this episode of Learners on Location, the assistant professor of Surgical Oncology and the fifth-year Pathology PhD candidate demonstrate how mentorship goes far beyond the lab. Their approach, grounded in wellness, growth, and purpose, demonstrate how personal wellbeing can lead to meaningful scientific impact.
Where's Wilmot's Director: Exploring the Cancer Microenvironment with Dr. Yeh's Lab
Friday, April 10, 2026
In April's installment of "Where's Wilmot's Director?", Dr. Jonathan Friedberg visted Shu-Chi (Allison) Yeh's lab in the CMSR. Dr. Friedberg met with Dr. Yeh and her multidisciplinary team to learn more about their insights and use of innovative technology in investigating the cancer microenvironment, a reasearch area of strength at Wilmot with new translational opportunities.
Click here to read more about Dr. Friedberg's visit to the Yeh Lab.
Gregg Nicandri Tapped to Lead New Digital Strategy & Innovation Office
Friday, March 20, 2026
URMC CEO David Linehan has named UR Medicine’s Chief Medical Information Officer Gregg Nicandri, MD, to lead the office as its inaugural Chief Digital & Innovation Officer (CDIO), charged with advancing an enterprise digital strategy to ensure innovation and execution are tightly aligned and positioned to deliver meaningful impact.
“We’re not running to catch up but leading the future,” said the new Chief Digital and Innovation Officer, who will work to advance an enterprise digital strategy, moving quickly and with intention to innovate and execute for meaningful impact. Linehan noted Nicandri’s experience has prepared him to forge our digital future. “He has worked tirelessly to develop innovative provider enablement tools to improve wellbeing by freeing up the time spent on administrative tasks to allow more quality face-to-face interactions with patients,” Linehan said.
Read about Dr. Nicandri's plans to propel the digital future of URMC.
Collaborative Effort Expands Upon Study Linking Taurine to Cancer
Friday, January 23, 2026
In a groundbreaking basic science study last year, researchers discovered that taurine, available in energy drinks and as a supplement, feeds the growth of leukemia stem cells. A new study recently published by the same Wilmot Cancer Institute team expands that work and suggests that as taurine fuels leukemia, it becomes less available for other normal cells and may result in weaker bones in mice.
The bone marrow microenvironment is key to the latest research from the Bajaj lab, and has been a longtime focus of scientists who are members of Wilmot’s Cancer Microenvironment (CM) research program. Not only do many types of cancer, including leukemia, develop in the bone marrow, but the interactions and signaling between all cells and tissues in the bone marrow environment are critical for normal bone and blood development, while also supporting cancer.
PhD candidate Christina M. Kaszuba, a student in the University of Rochester Biomedical Engineering graduate program, led this project. She works exclusively in the Bajaj lab studying cells and components of the bone that contribute to cancer development, with the goal of finding new cancer drugs.
Bajaj is an assistant professor of Biomedical Genetics and a recipient of an American Society of Hematology Scholar Award and Leukemia Research Foundation New Investigator Award.
The research, funded by the National Institutes of Health (NH) is the result of a broad collaboration that also includes Laura Calvi, MD, professor of Medicine and co-director of the CM research program; Jane Liesveld, MD, professor of Medicine; Hani Awad, PhD, professor of Orthopedics; Roman Eliseev, MD, PhD, associate professor of Orthopedics; and teams at the University of Rochester Center for Musculoskeletal Research and Wilmot Shared Resources.