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Trailblazing Minds In Science: Leonardo M. R. Ferreira, Ph.D.

Introduction

Leonardo M. R. Ferreira, Ph.D. is an Assistant Professor of Microbiology and Immunology and, by courtesy, of Regenerative Medicine and Cell Biology at the Medical University of South Carolina and the Hollings Cancer Center. He holds a B.Sc. in biochemistry from University of Coimbra, Portugal, and a Ph.D. in biochemistry from Harvard University. Fascinated by the phenomenon of immune tolerance, his long-term goal is to control how the immune system defines self and non-self. Such knowledge will allow the design and development of powerful new engineered immune cell therapies to fight autoimmune disease, cancer, and aging.



Headshot
Leonardo M. R. Ferreira

Thank you for speaking with us, Leonardo! Could you tell us more about your current role as an Assistant Professor of Microbiology and Immunology at the Medical University of South Carolina (MUSC) and the Hollings Cancer Center?


My current role as Assistant Professor is the culmination of thirteen years of training, starting when I first entered a research lab as a college freshman in Coimbra, Portugal. It is a very multifaceted occupation and there is a lot of deep thinking and planning involved, but also a lot of action. No two days are alike.


I ponder, design, write, and submit projects for funding. This includes finding out how much each reagent and salary costs, a budgeting exercise that is informed by but also informs the planned research. I design and perform experiments and analyse the resulting data. I still have a project or two in the lab that I drive. This is not only because actively doing research is just too much fun, I have way too many questions that I want to answer, and nothing can quite replace the thrill of discovery, but also because I believe it makes me a better and more reasonable mentor and grant writer.


The world of paperwork and grants has many deadlines that completely ignore that most cells take one day to double, and mice take twenty-one days to be born. By continuing to do experiments, I stay grounded and in tune with the rhythms of biology. I also sit in committees that evaluate other people’s grants, both internal and external, and publications, in addition to being editor and peer reviewer for other people’s manuscripts at scientific journals and being part of organizing committees for retreats and conferences.


I teach graduate school and medical school lectures, and co-direct the graduate-level immunology course. I recruit and mentor PhD students, medical students, undergraduate students, and high school students. That is a very important aspect of my role, as no single pair of hands can fulfil one’s vision and part of what makes academic science so special is that many times research problems can only be solved when ideas and execution from different backgrounds, perspectives, and levels of expertise come together. Such mentor-mentee relationships extend beyond the time they spend in my lab, which has now been around for long enough that some of my former trainees are applying to their next steps (medical school, pharmacy school, PhD programs).


Another aspect of my role that I enjoy is the opportunity to collaborate with other faculty and labs, both locally and elsewhere in the world. This has provided for many stimulating conversations and exciting data.



"My PhD research got me fascinated with controlling the immune system and immune tolerance induction and allowed me to gene edit primary human T cells and stem cells."


Could you share a bit about your background?


I wanted to be a scientist since an early age. I marvelled at the fact that the wounds in my knees would heal back every time I fell playing soccer and wondered what was behind it, so blood and regeneration were concepts that left an impression on me early on. While in high school in the science track, I went to the city library and started opening books in the college textbook section in the hopes of finding help deciding what major to pick in college. The book that startled me the most was the organic chemistry textbook, especially the page with a structure of cellulose. Such a complex biological molecule, and yet we seemed to know every atom of it and the magnitude of every angle it made with its neighbouring atoms.


Craving that level of understanding of the biological world, I studied biochemistry at the University of Coimbra in Portugal and did research in laboratories working on cancer metabolism, organic synthesis, nuclear magnetic resonance, plants, and molecular biology.


As you reflect on your journey from biochemistry in Portugal to transitioning to researching immunology, what drew you to the complexities of the immune system?


It has been a long journey, intellectually speaking. As a freshman in biochemistry in Portugal, I did not imagine I would be doing research in immunology at the Harvard Stem Cell Institute as a graduate student. During college, my main fascination changed from organic chemistry, where structure determines function, to genetic engineering, which allows one to rewrite the code of life, to stem cells, which can become any cell type in the body. It was with stem cell research and regeneration in mind that I applied to PhD programs in the United States and how I ended up rotating in labs at Harvard’s Department of Stem Cell and Regenerative Biology (HSCRB) and Stem Cell Institute (HSCI).


One of these rotations was in the lab of Jack Strominger (my PhD advisor), an esteemed immunologist who contributed to the first structure of a major histocompatibility complex (MHC) molecule, human leukocyte antigen A2 (HLA-A2), elucidating how a T cell receptor (TCR) binds to a peptide-MHC complex, and many other fundamental aspects of immunology. And the rest is history.


I became fascinated with the problem of self-nonself recognition, how our immune system can tell them apart and how so many problems arise when this recognition system goes awry. Misplace cancer neoantigens in the self category, and you are not able to eliminate tumours. Misplace beta cell antigens in the nonself category, and you eliminate beta cells and become unable to produce insulin and control blood sugar.


Moreover, the promise of stem cell research and regenerative medicine seemed to have a partial caveat: take someone’s cells and transplant them into someone else to replace the damaged cells or tissues, and the recipient’s immune system will reject those therapeutic cells. Being able to control self-nonself recognition by the immune system thus became an obsession of mine.


Of note, I had never taken a single immunology course or even read much about the topic before rotating in the Strominger Lab, which I think just underscores how full of possibilities the first year of graduate school, at least in the United States, is, where serendipity and finding one’s true passion are the top priorities.



Graphical abstract
Graphical abstract | Mandal et al. 2014

How did you first become interested in Tregs?


During my PhD, in addition to working on CRISPR/Cas9 genome editing in T cells (back when we electroporated plasmid DNA coding for Cas9 and guide RNAs into human T cells ("Efficient Ablation of Genes in Human Hematopoietic Stem and Effector Cells using CRISPR/Cas9"), I worked on pregnancy immunology.


A fascinating topic and an enigma in immunology. The foetus is 50% to the mother and yet does not get rejected for nine months. But if you take a skin graft from the father and transplant it into the pregnant mother’s skin, it gets rejected. Pregnant women’s responses to vaccines also seem unaffected. In fact, pregnant women generate antibodies against paternal HLA molecules in the foetus.


It is known that foetal extravillous trophoblasts (EVT), which invade the uterus during implantation, express a different repertoire of immune molecules than most cells in the body, including the tolerance inducing nonclassical MHC molecule HLA-G. It is also known that the maternal-foetal interface has a very different immune composition from peripheral blood, with decidual Natural Killer (NK) cells being much more numerous and displaying a different phenotype from peripheral blood NK cells. While this is clearly the perfect example of local long-lasting immune tolerance to transplantation antigens, it is hard to put the maternal-foetal interface in a test tube, let alone somehow transferring it into another human.


But regulatory T cells (Tregs), this subset of cells that inhibits immune responses using over a dozen different mechanisms, can be sorted with high purity from blood into a test tube, genetically modified, expanded, and infused into the same or another human to induce immune tolerance. Brilliant!


What specific experiences or moments shaped your decision to focus on autoimmune diseases and Treg cell therapy?


My first exposure to autoimmune disease, specifically type 1 diabetes (T1D), was as a rotation student in Doug Melton’s laboratory, which focused on differentiating functional beta cells from pluripotent stem cells. This intense focus on fulfilling the promise of stem cell research in the context of an autoimmune disease, where one must not only replenish the lost cells, but also prevent them from being destroyed like their precursors were, certainly left an impression on me.


When it was time to search for a postdoctoral fellowship four years later, I interviewed with Qizhi Tang and Jeff Bluestone, Treg pioneers at the University of California San Francisco (UCSF). The ongoing research in their labs at the basic and translational levels, the literal physical bridge between the stem cell research building and the research building where immunology labs are located at UCSF, and the foggy city of San Francisco got me instantly hooked and I joined their lab to learn the ways of Treg cell therapy and autoimmune disease research.


My PhD research got me fascinated with controlling the immune system and immune tolerance induction and allowed me to gene edit primary human T cells and stem cells. During my postdoctoral fellowship, I isolated human Tregs and not only gene edited them, but also augmented them with chimeric antigen receptors we developed for new targets and featuring new signalling domains. It was also then that I started working with humanized mouse models to put these engineered cells to test in vivo.


The excitement of making living drugs out of Tregs and putting them to test prompted me to focus on Tregs and autoimmune disease.



"Science really is mostly a marathon, not a sprint. This does not mean that one does not have to sprint sometimes, and that is part of the fun in science for some of us, the race, the not being able to wait until tomorrow to find the answer and tell the world."


Group of people
The Ferreira lab

Could you give us an overview of the current research happening in your lab?


My laboratory works on designing and developing engineered Tregs as living drugs for autoimmune disease, cancer, and aging. I feel fortunate and, frankly, proud, that I have been able to build over the past two years a lab where a diverse group of people with experience spanning various degrees, from high school students to advanced PhD students, address research questions using techniques spanning from molecular biology to mouse models.


I think this is important because it allows a more complete understanding a control of each project. To work with engineered immune cells, it is important to not only be an expert in cell culture and flow cytometry, but also understand each element of the DNA constructs used to engineer the immune cells, as well as to test the cells not only in vitro but also in experimental animals. Part of our work involves designing new artificial immune receptors and we use both human and mouse cells in our studies.


What are some of the challenges your lab faces in developing these Treg cell therapies, and how do you navigate them?


There are several challenges to surpass when developing Treg therapies. Some of them can be grouped into obtaining enough Tregs for our studies. Since Tregs are only 1% of peripheral blood mononuclear cells (PBMCs) and divide more slowly than conventional T cells, Tregs numbers are always in the back of our minds, especially when using cells from the same blood donor to test different constructs or set up big in vivo experiments. These have to do with the blood source, isolation method, ex vivo expansion technique, and method used to modify the cells.


Others can be grouped into challenges testing Tregs. If using human Tregs in vitro, then it is possible that not all relevant immune cell types are present, or the duration of the experiment is inadequate. If using human Tregs in vivo, there can be reduced survival and persistence of the cells in immunodeficient NSG mice due to lack of immune cell subsets, lymph nodes, and appropriate cytokine levels. If using mouse Tregs in immunocompetent mouse models, then there is the risk that mouse cells and diseases do not always translate well into human cells and diseases, the ultimate goal of translational research.


How do you and your team stay inspired and motivated during challenging times?


It is very important to keep the focus as much in the process as in the result. Making new discoveries is thrilling. The importance of each discovery is something be found out later, maybe many years later. Likewise, failing an experiment or disproving one’s favourite hypothesis might not feel great in the moment, but there should still be learnings to be gleaned from the event.


Science really is mostly a marathon, not a sprint. This does not mean that one does not have to sprint sometimes, and that is part of the fun in science for some of us, the race, the not being able to wait until tomorrow to find the answer and tell the world. But challenging times will pass, and one keeps running the marathon, enjoying the view and having something to look forward to at the end of each project.


Often, it is better to take a break, reassess, and start fresh than to keep hammering on the same failing process. Sometimes the solution is not to keep trying to break into the door, but instead to go around and look for a window.



Medical University of South Carolina
Medical University of South Carolina

How does your lab collaborate with other research groups or organisations to advance crucial research?


My lab collaborates with labs at MUSC as well at other institutions in the United States. The goal of these collaborations is the reciprocal expansion of the technical expertise and field knowledge of each lab. Collaboration is important to create novel ideas and approaches and to enrich the trainees’ experiences.


Moreover, MUSC harbours a Good Manufacturing Practice (GMP) cell therapy facility, as well as a culture of collaboration between physicians, physician-scientists, and scientists like me and support for entrepreneurial faculty, expediting the testing of engineered immune cells in the clinic.


Do you think there should be more collaborations between Academia and Industry to progress innovative cell therapies?


Absolutely. Industry is essential to rigorously test and manufacture Treg cell therapies at scale. Academia and Industry tend to play very important but distinct, and often complementary roles in science. It also opens the doors to iterations, so familiar to those of us engineering immunology, where learning new basic immunology often goes hand in hand with attempts to engineer it.


Likewise, Industry can benefit tremendously from the discovery spirit of Academia, while Academia can learn a great amount about the implementation spirit of Industry. Immunology is an inherently translational field, with any given basic discovery invariably having the potential to impact human health. Immunology, and in particular research focused on Tregs, is thus uniquely poised to benefit from increased Academia-Industry partnerships.


Graphical abstract
CRISPR-Cas9 overview

What is your most rewarding or exciting moment in your research career?


The most rewarding and exciting moment in my research career thus far happened when I was in graduate school. It was a late weeknight and I was missing someone’s birthday party to be in the lab. I really had to get this answer. The year was 2013.


Earlier that year, it was shown that CRISPR/Cas9 could be used to introduce mutations and knockout genes in human cell lines in a specific manner. Since this work came out of the neighbouring Massachusetts Institute of Technology (MIT) and Harvard Medical School, I had access to those first plasmids early on and was able to use them to ask one of my research questions. I was working on the transcriptional regulation of HLA-G, a nonclassical nonpolymorphic MHC molecule expressed exclusively in foetal extravillous trophoblasts (EVT) and thought to play a key role in maternal-foetal tolerance, as it inhibits natural killer (NK) cells and does not activate T cells.


In fact, EVT have a unique HLA molecule expression pattern; they selective silence expression of the ubiquitous polymorphic HLA-A and HLA-B while uniquely expressing HLA-G. We had just run an experiment that suggested there was a 100-base-pair-long regulatory region, an enhancer, 10,000 base pairs upstream of the HLA-G gene. If it were really important, I reasoned, deleting it from the genome should affect HLA-G expression. So I took an EVT cell line, transfected the cells with Cas9 and guide RNAs flanking that putative 100 bp enhancer region to crop it out, selected single-cell derived homozygous deletion clones and wild-type clones and ran flow on HLA-G surface expression on the clones that night. HLA-G gene expression was not reduced in the 100 bp region deletion clones, it was completely gone! Still my favourite experiment to this day.


In the Treg world, my most exciting moment happened when I was a postdoctoral fellow. The promise of CAR Tregs is that they are laser focused cells that migrate to the site of interest and accumulate them. So it was really satisfying to see our luciferase-labeled HLA-A2 CAR Tregs trafficking to and remaining in the HLA-A2-positive human islet graft in the kidney capsule in NSG mice for over two weeks, while luciferase-labeled polyclonal Tregs disappeared after a few days.



"Treg cell therapies are going to transform autoimmune disease treatment by providing a treatment modality that is precise and addresses the root cause of the disease."


What are some of the areas within Treg biology that we need to understand better to improve the next generation of Treg cell therapies?


A big area of Treg biology that we need to delve deep into is the characterization of tissue-specific Tregs. While most studies utilize peripheral blood Tregs, most of the immune action happens in the tissue.


The picture that has been emerging is that different tissue-resident Treg subsets play important, sometimes even unexpected, roles. Adipose tissue Tregs influence metabolic control by adipocytes. Muscle Tregs are important to limit damage to mitochondria after physical exercise and are required for muscle gains. Skin Tregs secrete factors that induce the proliferation of hair follicle stem cells. It thus stands to reason that we have a lot to learn about different Treg subsets to find the ideal one for each disease indication that Tregs can potentially help with.


Another area to focus on is the genetic engineering of Tregs with artificial receptors, such as chimeric antigen receptors (CARs), cytokine converters, and biosensors for inflammation to redirect and expand their function. A lot is known about how CARs function in conventional T cells – affinity, hinge domain, signalling domain, target expression level, and so on – but the same is not true yet in Tregs.


Moreover, while CAR T cells for cancer therapy are, at least at first glance, limited to target molecules expressed on the cancer cells to be eliminated, CAR Tregs could, in theory, target the tissue cells to be protected, the antigen-presenting cells priming the aggressor T cells, the aggressor T cells themselves, or even the extracellular matrix of the tissue to be protected. These are important to iron out as we continue to develop and test engineered Tregs as living drugs.


The next generation of Treg cell therapies use genetic engineering to enhance the Tregs. What are some mechanisms or functions of Tregs that you believe would benefit from such genetic enhancements?


I see engineered Tregs as living drugs that, to be successful, should observe what I call the 4S:

  • Specificity

  • Survival

  • Stability

  • Suppression


The first S, Specificity, can be enhanced by redirecting Tregs with artificial receptors, such as a CAR or a transgenic T cell receptor (TCR). The second S, survival, can be enhanced by gene modifications affecting cell survival pathways and cytokine converters where Tregs are led to believe they are exposed to ample interleukin-2 (IL-2). The way Tregs are cultured ex vivo may also impact their survival in vivo, as well as some other gene manipulations, either permanent or transient, such as those impacting STAT5 signalling, key to cell engraftment.


The third S, stability, can also be enhanced by cytokine converters where Tregs are led to believe they are exposed to IL-2 or artificial orthogonal cytokine receptors that respond to an artificial orthogonal cytokine infused in the patients. Moreover, Stability can benefit from engineering of the FOXP3 locus to stabilize gene expression and modulation of additional transcriptional and epigenetic regulators.


The fourth S, Suppression, is perhaps the hardest one to enhance, given the multitude of suppressive mechanisms that Tregs can employ depending on the scenario and on the Treg subset, and because it is not trivial that increasing expression of CD25 or CTLA4 or CD39 would necessarily increase suppressive function on a per cell basis.


Still, it may be beneficial to include gene circuits to ensure anti-inflammatory cytokine production by engineered Tregs upon local activation. There are also some data suggesting that higher affinity TCR Tregs may be more suppressive than lower affinity TCR Tregs. Given Tregs’ requirement for stimulation for survival and function, Specificity might well be the most important of the 4S. With the right Specificity, the engineered Tregs will traffic to the desired location, become stimulated, survive, remain stable, and suppress immune responses via bystander suppression and infectious tolerance.


There is a fifth S that will also be important – Safety. Given the higher safety bar for autoimmune disease therapies than, for example, therapies targeting malignant tumours, it is key to ensure that infused engineered Tregs do not become unstable and convert into pro-inflammatory cells and/or acquire de novo pro-inflammatory properties. Moreover, it will be important that the target is very specific, as to not inadvertently protect tumour formation from immune surveillance offsite.



Graphical abstract
Overview of common autoimmune diseases

How do you envision Treg cell therapies transforming the landscape of autoimmune disease treatment globally?


Treg cell therapies are going to transform autoimmune disease treatment by providing a treatment modality that is precise and addresses the root cause of the disease.


Moreover, Treg therapies are amenable to be combined with other approaches. For systemic lupus erythematosus (SLE), for example, ongoing low-dose IL-2 therapy, which aims to boost endogenous Tregs, can be combined with the administration of ex vivo expanded Tregs. For type 1 diabetes (T1D), Treg infusions may be combined with transplanted islets to replenish the lost beta cell mass and help protect the therapeutic cells.


This vision depends on our capacity to generate high quality Tregs specific to a relevant antigen. In the T1D space, a target that is being pursued is HLA-A2, as HLA-A2 CAR Tregs could specifically protect HLA-A2 positive pancreatic islets transplanted into an HLA-A2 negative T1D recipient. Trials in the graft-vs-host disease and organ transplantation spaces, historically precursors for trials in the autoimmune disease space as far as Treg therapies go, are currently under way for HLA-A2 CAR Tregs.


Another aspect worth mentioning is that, unlike immunosuppressive drugs or insulin, which must be taken daily, Treg therapy would be administered once or seldom, if Tregs are to fulfil the promise of re-educating the immune system to induce long-lasting immune tolerance towards a previously immunogenic target.


In your expert opinion, what do you predict the next decade holds for Treg cell therapy and autoimmune disease treatment?


The next decade will be a very exciting one for Treg-based therapies and autoimmune disease treatment. A lot of cell therapy approaches and methodologies are starting to prove themselves in the clinic. There are now half a dozen FDA-approved chimeric antigen receptor (CAR) T cell therapies for liquid tumours. Islet transplant for type 1 diabetes was approved by the FDA this year. There are results from a trial with transplanted encapsulated islets and trials with genetically engineered hypoimmunogenic islets are starting. The first CRISPR-based therapy in the world, for sickle cell anaemia, was approved in the UK this year.


The CAR Treg subfield has had more publications in the past two years than in all previous years combined. Treg-centric companies like Sonoma Biotherapeutics, Quell Therapeutics, GentiBio, Bastion Therapeutics, and others have investigational new drugs (INDs) and trials. Work on making Treg cell therapy a reality for a number of indications is thus happening at full steam. I believe this decade will see the first approved Treg therapy.



"I see a Treg as a hyper social, gregarious, and possibly self-centred and a bit controlling, cell type. Is there any immune cell type that Tregs don’t influence?"


Can you foresee specific autoimmune diseases being positively impacted by Treg cell therapies in the near future?


Type 1 diabetes will be positively impacted by Treg cell therapies. There are very strong preclinical data in the nonobese diabetic mouse since the early 2000s that antigen-specific Tregs can prevent and even revert type 1 diabetes and there are clinical data from the 2010s that it is safe to infuse up to 3 billion Tregs in type 1 diabetes patients. There are also encouraging preclinical results using human and mouse CAR Tregs to prevent type 1 diabetes.


The fact that a curative treatment for type 1 diabetes is pancreas or pancreatic islet transplant also makes type 1 diabetes potentially more tractable than other autoimmune diseases, as it can draw from the past and ongoing research on tolerizing organ transplants in addition to the work in the autoimmune space.


Another autoimmune disease that may also benefit from Treg cell therapies in the near future is multiple sclerosis, given the sharply accelerating interest in studying the role and utilization of Tregs in neurodegenerative diseases.


How do you think this will impact the lives of individuals with autoimmune conditions and their loved ones on a personal level?


Treg therapies have the potential to tremendously impact the lives of autoimmune disease patients and their families by providing an efficacious treatment, potentially even a cure, and a peace of mind not afforded by current treatments.


The triggers and targets of autoimmune disorders are many times unknown. One of the beauties of Treg-based therapies is that you might not need to know either for a successful treatment. For instance, in type 1 diabetes, the target of autoimmune attack is the pancreatic islets. Administering engineered Tregs that traffic to the pancreas will abolish the ongoing local inflammation there irrespective of what caused the disease or what antigens the disease-causing autoreactive T cells target.



"Immunology happens to not only provide an ample source of questions, but also the type that, if answered, can change the human condition."



On a lighter note, if Tregs had personalities, what do you think they would be like?


I see a Treg as a hyper social, gregarious, and possibly self-centred and a bit controlling, cell type. Is there any immune cell type that Tregs don’t influence?


Tregs inhibit immune responses using over a dozen different mechanisms. If they see IL-2 floating around, they soak it (with CD25) so there is none left for conventional T cells. If they see CD80 or CD86 on antigen-presenting cells, they take it to themselves (with CTLA4). If there’s ATP floating around, they convert it into adenosine (via CD39 and CD73), effectively transforming a pro-inflammatory signal to an anti-inflammatory signal. It’s as if the whole immune system revolves around the Treg!


But the Treg is also caring. After all, its job is to make sure that no immune response goes so overboard that it damages healthy tissue. And Tregs even help heal (via amphiregulin) injured tissue!


It’s been a pleasure to speak with you, Leonardo. Thank you for sharing your insights and expertise. It’s been fascinating to delve into your world.


Thank you for the opportunity to share some of my thoughts. I have a lot of questions that I want to answer, and I feel privileged that I get to work on answering those questions every day for a living. Immunology happens to not only provide an ample source of questions, but also the type that, if answered, can change the human condition.


Website still
The Ferreira Lab website

We're sure our audience would be interested in staying updated on your lab's work. Where can they find more information or follow your latest discoveries?


I was fortunate that the domain ferreiralab.com had not been acquired yet in 2020 when I started applying for faculty positions, so my lab website is https://www.ferreiralab.com/.


It features lab members, publications, lab protocols, teaching materials (PowerPoint slides from lectures, links to webinars and interviews), funding, and a gallery of photos of the group as the time goes by (last one is from Halloween 2023, or Day 852 of the lab’s existence). I announce lab milestones on social media platforms, including Twitter/X, LinkedIn, Facebook, and Instagram. Links to my pages below. Otherwise, nothing like running into one another at a conference!



Some publications representative of my work on engineered Tregs thus far, working towards adding a couple more in 2024:


1. Ferreira#, L.M.R., Muller#, Y.D., Bluestone, J.A., Tang, Q., 2019. Next-generation regulatory T cell therapy. Nat Rev Drug Discov 18, 749-769


2. Muller#, Y.D., Ferreira#, L.M.R., Ronin, E., Ho, P., Nguyen, V., Faleo, G., Zhou, Y., Lee, K., Leung, K.K., Skartsis, N., Kaul, A.M., Mulder, A., Claas, F.H.J., Wells, J.A., Bluestone, J.A., Tang*, Q., 2021. Precision engineering of an anti-HLA-A2 chimeric antigen receptor in regulatory T cells for transplant immune tolerance. Front Immunol 12:686439.


3. Ghobadinezhad, F., Ebrahimi, N., Mozaffari, F., Moradi, N., Beiranvand, S., Pournazari, M., Rezaei-Tazangi, F., Khorram, R., Afshinpour, M., Robino, R.A., Aref*, A.R., Ferreira*, L.M.R., 2022. The emerging role of regulatory cell-based therapy in autoimmune disease. Front Immunol 13:1075813


4. Zimmerman, C.M., Robino, R.A., Cochrane R.W., Dominguez, M.D., Ferreira*, L.M.R., 2024. Redirecting human conventional and regulatory T cells using chimeric antigen receptors. Methods Mol Biol 2748:201-241


# Co-first author

* Corresponding author

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