Inflammation is a critical response to potential danger signals and damage in organs in our body. But with autoimmune diseases such as rheumatoid arthritis, lupus, ulcerative colitis, Crohn’s disease and many others, our own immune system turns against our organs. These painful and debilitating conditions take an immense toll on people’s quality of life and many of these diseases are poorly managed by existing treatments that provide only symptomatic relief.
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Immunology and Inflammation Research and Development
Inflammation is a critical response to potential danger signals and damage in organs in our body.
Iain Kilty: What We’re Working on
For decades, doctors relied on steroids to suppress immune response. Though an important option, steroids come with many potentially harmful side effects. Fortunately, science has continued to advance, and today we have the opportunity to transform the management of inflammatory diseases with new classes of therapies that target other key proteins and pathways in the body.
As science evolves beyond broad immunosuppression and into more selective agents, patients living with autoimmune and inflammatory disease have new hope.
As science evolves beyond broad immunosuppression and into more selective agents, patients living with autoimmune and inflammatory disease have new hope. Pfizer scientists operate with a sense of urgency, focused on three areas with the greatest unmet need:
Rheumatology Investigating therapies for rheumatoid arthritis and lupus
Gastroenterology Looking at the next wave of medicines in ulcerative colitis, Crohn’s disease and nonalcoholic steatohepatitis (NASH)
Medical Dermatology Focusing on the next generation of medicines for atopic dermatitis, psoriasis, vitiligo and alopecia areata
Innovation in I&I will remain focused on enabling patients to thrive in remission and to attain cures. It is believed that in the longer term, this will be achieved by evolving the treatment paradigm in inflammation beyond broad immunosuppression. In the clinic, more selective inhibition of pro-inflammatory adaptive pathways is being targeted to deliver transformational induction and maintenance of remission with lower safety risks. Emerging approaches are aimed at promoting restoration of the immune system and tissue health to deliver cures.
Emerging approaches are aimed at promoting restoration of the immune system and tissue health to deliver cures.
Precision medicine is embedded in all of our investigational programs in Inflammation and Immunology, where we seek to better understand the underlying disease biology and identify the group of patients who will respond best to certain treatments. Pfizer sees particular promise in combination therapies to reduce remission rates.
Technologies/Approach
JAK pathwayOur janus kinase (JAK) inhibitor programs are at the heart of our R&D efforts in a number of autoimmune diseases in addition to rheumatoid arthritis. We’re advancing our leading science on the JAK pathway to develop tailored therapies for lupus, psoriasis, ulcerative colitis and alopecia areata – all areas in which we have ongoing clinical trials.
Immune ToleranceActivation of the immune system by self-antigens is the basis of every autoimmune disease. Immunological tolerance is the term describing a host of normal physiological processes to prevent this activation from happening. Current treatments for autoimmune diseases result in broad immunosuppression, occasionally resulting in infection or insufficient tumor surveillance. We believe the future of treatment for autoimmune disease is specific restoration of self-tolerance rather than immunosuppression, and have established a group in R&D dedicated to this effort.
Big data Every day we generate massive amounts of data in our clinical trials and laboratory experiments that enable us to describe diseases in greater and greater detail. The data includes both how patients and clinicians describe symptoms and response to treatment as well as data that describes the effects a drug has on the body’s molecular and cellular mechanisms. Together this forms a unique knowledge database. With the help of advanced analytics we are able to interrogate this “Big Data” to drive our understanding what targets and pathways may best help resolve disease and what treatment would be best for each patient.
Collaborations
23andMeSince 2014, Pfizer and 23andMe have engaged in an expanding collaboration to help foster research in several different autoimmune and inflammatory diseases including lupus, ulcerative colitis and Crohn’s disease. Our work explores the underlying genetic factors associated with these diseases in the hope of developing new or improved treatments. In addition to enrolling over 15,000 individuals within two separate research initiatives focused on inflammatory bowel disease and lupus, respectively, our most recent partnership gives Pfizer access to 23andMe’s unique research platform and analysis of the company’s genotyped population of over 800,000 individuals who have consented to participate in research. This wealth of patient data offers yet another opportunity to better understand potential links between genetic traits and disease.
BioRapPfizer recently entered into a collaboration, option and license agreement with BioRap Technologies, Ltd., the technology transfer company of the Rappaport Institute of Biomedical Research at the Technion – Israel Institute of Technology. The collaboration is based on work of Dr. Nathan Karim at the Rappaport Institute who has developed a monoclonal antibody that appears to drive the development activity of regulatory T cells – a cell type that plays a role in controlling autoimmunity. This antibody may offer a new potential treatment for certain autoimmune diseases, including inflammatory bowel disease (IBD) and multiple sclerosis (MS).
Work with Us
If you’re interested in collaborating with our Inflammation and Immunology teams, visit our Immunoscience Partnering and Inflammation and Immunology pages to learn more about the work we’re pursuing.
Meet Some of Pfizer’s Inflammation and Immunology Researchers
Jean Beebe, PhD
Vice President, Clinical Portfolio Leader, I&I Research Unit
- Group: Inflammation & Immunology
- Location: Cambridge
- LinkedIn page URL: https://www.linkedin.com/in/jean-beebe-98446610/
I am a Clinical Portfolio Leader in the Inflammation and Immunology Research Unit with over 25 years of experience in drug discovery and development at Pfizer. I began my career at Pfizer in the oncology discovery labs in Groton. I had roles of increasing responsibility including leadership of Discovery biology efforts for oncology, immunology and antibacterial research and Team leader for oncology assets in clinical development.
In my current role, I lead the development teams that are responsible for milestones from First-in-Human through Proof-of-Concept for both biologic and small molecule approaches for Inflammation and Immunology assets. I am tremendously proud of my teams’ achievements, including most recently, the JAK1 asset that achieved Proof-of-Concept in atopic dermatitis including a Phase 3 start in 2017.
I earned my BS degree in Biochemistry from the University of Vermont and my Ph.D in Molecular Pharmacology from the University of Michigan.
RESEARCH AREA(S)
The teams who work in the early development space are accountable for milestones from First-in-Human through Proof-of-Concept. Team members bring valuable perspectives from their lines and work tirelessly to ensure we assemble the most efficient strategies to test our scientific hypotheses in humans.
These teams assemble development plans that include precision medicine approaches that allow us to quantitate the pharmacodynamic activity of our compounds and to understand the patient populations that may have the best response to our drug. We explore a variety of disease areas in the Inflammation and Immunology RU that includes Systemic Lupus Erythematosus, lupus nephritis, atopic dermatitis, rheumatoid arthritis, to name a few.
The culture of the teams is really important to me – I want team members to be empowered to challenge our assumptions, raise issues and concerns, and to take risks as well as to be efficient with our spending – this is so important to ensure we bring the best plans forward.
PUBLICATIONS
- Increased Serum Enzyme Levels Associated with Kupffer Cells Reduction with No Signs of Hepatic or Skeletal Muscle Injury. American Journal of Pathology 179:240-7, 2011. Radi, ZA, Koza-Taylor, PH, Bell RR, Obert L, Giovanelli RP, Runnels HA, Beebe JS, Lawton MP, Sadis, S https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3123844/
- Anti-IL21 receptor monoclonal antibody (ATR-107): Safety, pharmacokinetics, and pharmacodynamic evaluation in healthy volunteers: a phase 1, first-in-human study. J Clin Pharm 54(1): 14-22, 2014. Hua F, Comer GM, Stockert L, Jin B, Nowak J, Pleasic-WilliamsS, Wunderlich D, Cheng J, Beebe JS
- Efficacy and safety of an interleukin 6 monoclonal antibody for the treatment of systemic lupus erythematosus: a phase II dose-ranging randomised controlled trial. Ann Rheum Dis76: 534, 2017 Published Online First [Sept 26, 2016] doi:10.1136/annrheumdis-2016-209668. Wallace DJ, Strand V, Merrill JT, Popa S, Spindler, AJ, Eimon A, Petri M, Smolen JS, Wajdula J, Christensen J, Li C, Diehl A, Vincent MS, Beebe J, Healey P, Sridharan https://www.ncbi.nlm.nih.gov/pubmed/27672124
- Randomized trial and open-label extension study of an anti-interleukin-6 antibody in Crohn’s disease (ANDANTE I and II) Gut Published online First [Dec 15, 2017] doi:1136/gutjnl-2017-314562. Danese S, Vermeire S, Hellstern P, Panaccione R, Rogler G, Fraser G, Kohn A, Desreumaux, P, Leong RW, Comer GM, Cataldi F, Banerjee A, Maguire MK, Li C, Rath N, Beebe J, Schreiber S https://www.ncbi.nlm.nih.gov/pubmed/29247068
- PF-04965842, a JAK1 inhibitor, for treatment of atopic dermatitis: a 12-week, randomised, double-blind, placebo-controlled phase 2 clinical trial. Late-breaker abstract at 2017 EADV conference, Geneva. Gooderham M, Forman S, Bissonnette R, Beebe J, Zhang W, Banfield C, Zhu L, Papacharalambus J, Vincent M, Peeva E
EDUCATION
University of Vermont, Burlington, Biochemistry B.S., 1984
University of Michigan, Ann Arbor, Molecular Pharmacology, Ph.D., 1989
QUOTE
“I joined Pfizer because I was so impressed with how the scientists worked together in multidisciplinary teams and are united in a common goal of bringing new medicines to patients. I have stayed at Pfizer because I have the privilege of working with so many exceptional colleagues and so many opportunities to learn. And because I am fully committed and all-in on our mission to develop new innovative medicines.”
Jeremy D Gale, PhD
Vice President and Clinical Portfolio Leader
- Group: Inflammation & Immunology
- Location: Cambridge, MA
- LinkedIn page URL: https://www.linkedin.com/in/jeremygale
I am Vice President and Clinical Portfolio Leader in the Pfizer Inflammation and Immunology Research Unit in Cambridge, Massachusetts. I joined Pfizer in 1995 to lead the Gastrointestinal Discovery Biology group at the Sandwich site in the UK and then joined the Experimental Medicine group in 2002. Prior to this I worked for Glaxo as a Research Leader in the Gastrointestinal Pharmacology Group. Since joining the clinical world I have led early clinical development and translational medicine activities from first-into-human to clinical proof-of-concept across a range of diverse diseases in gastroenterology and hepatology. Since 2008, I have been leading clinical development activities across several areas of internal medicine, including nephrology, as either RPL or Clinical Lead. I currently have responsibility for early clinical development activities in Inflammatory Bowel Disease.
RESEARCH AREA(S)
My research focuses on the early clinical development of novel medicines, primarily in the field of gastroenterology, but also nephrology, skin scarring, complications of diabetes and women’s health. The scope of my research is Phase 1 to Phase 2b and includes biomarker-based and translational medicine-based approaches to decision making.
PUBLICATIONS
- Scheele W, Diamond S, Gale J, Clerin V, Tamimi N, Le V, Walley R, Grover-Páez F, Perros-Huguet C, Rolph T and El Nahas M (2016) Selective inhibition of phosphodiesterase type 5 reduces albuminuria in subjects with type 2 diabetes and overt nephropathy. J Am Soc Nephrol 27(11):3459-3468. https://www.ncbi.nlm.nih.gov/pubmed/27113485
- Walley R.J, Birch C.L, Gale J.D and Woodward P (2015) Advantages of a wholly Bayesian approach to assessing efficacy in early drug development: a case study. Pharm Stat 14: 205-215. https://www.ncbi.nlm.nih.gov/pubmed/25865949
- Manousou P, Burroughs A.K, Tsochatzis E, Isgro G, Hall A, Green A, Calvaruso V, Ma G.L, Gale J, Burgess G, O'Beirne J, Patch D, Thorburn D, Leandro G, and Dhillon A.P. (2013) Digital image analysis of collagen assessment of progression of fibrosis in recurrent HCV after liver transplantation. J Hepatol 58(5): 962-8. https://www.ncbi.nlm.nih.gov/pubmed/23262247
- Gale, J.D and Houghton L.A (2011) Alpha2delta (2) ligands, gabapentin and pregabalin: What’s the evidence for potential use of these ligands in irritable bowel syndrome. Frontiers Gastrointestinal Pharmacology 2:1-9 https://www.ncbi.nlm.nih.gov/pubmed/21713059
- Ferens D.M, Yin L, Ohashi-Doi K, Habgood M, Bron R, Gale J.D. and Furness J.B (2010) Evidence for functional ghrelin receptors on parasympathetic preganglionic neurons of micturition control pathways in the rat. Clin Exp Pharmacol Physiol 37: 926-932. https://www.ncbi.nlm.nih.gov/pubmed/20497419
- Neubert H, Gale J, Muirhead D (2010) Quantitative Protein Bioanalysis by Online High Flow Peptide Immunoaffinity Enrichment and Nanoflow LC-MS/MS: Assay Development for Measuring Total Salivary Pepsin/Pepsinogen. Clin Chem 56: 1413-1423.https://www.ncbi.nlm.nih.gov/pubmed/20472821/
EDUCATION
European Confederation of the Upper Rhine Universities, Basel, Freiburg & Strasbourg, Diploma and University Professional of Advanced Studies in Pharmaceutical Medicine, European Center of Pharmaceutical Medicine, 2015
University of Warwick, 2011
University of London, Royal Free Hospital School of Medicine, Ph.D: “Morphological and pharmacological studies of 5-HT in sympathetic nerve fibres,” 1988
Sunderland Polytechnic, Sunderland, Pharmacology, Class II (i), B.S. (Honors), 1985
AWARDS & HONORS
Honorary Professorship, University of Liverpool, 2015 – 2018
Postgraduate Award in Management of Chronic Kidney Disease (Obtained a 67% overall), University of Warwick, 2011
Graduated in top 25% of class in 4/5 modules, European Confederation of the Upper Rhine Universities, Basel, Freiburg & Strasbourg, 2003-2005
Michael S. Vincent, MD, PhD
Senior Vice President, Chief Scientific Officer
- Group: Inflammation & Immunology
- Location: Cambridge, MA
Mike Vincent, MD, PhD, is Senior Vice President and Chief Scientific Officer of the Inflammation and Immunology Research Unit, leading the scientific pipeline for Rheumatology, Gastroenterology and Dermatology specialties through the end of phase 2.
Dr. Vincent earned his BA, PhD, and MD degrees from Indiana University. He completed his residency and began his post-doctoral and rheumatology training at the University of Vermont, completing his fellowship at Brigham and Women’s Hospital. His research while on faculty at Harvard centered on human T cell-dendritic cell interactions, and basic mechanisms of autoimmunity.
Since joining Pfizer in 2011, he has held several scientific leadership roles, most recently as Clinical Head for Pharmatherapeutics in Cambridge, MA. Over this period, he has had responsibility for clinical and translational science in the Inflammation and Immunology, Rare Disease and the Cardiovascular and Metabolic Disease Research Units, and the Centers for Therapeutic Innovation.
Before joining Pfizer, Dr. Vincent held positions of increasing responsibility within Medical Sciences at Amgen, ultimately leading early clinical development for the Immunology and Neuroscience therapeutic areas.
Thomas A. Wynn, PhD
Vice President, Discovery
- Group: Inflammation and Immunology
- Location: Cambridge, MA
- LinkedIn page URL: https://www.linkedin.com/in/thomas-wynn-251b43/
In July 2017, I joined Pfizer to lead the Discovery effort in the Inflammation and Immunology Research Unit at Pfizer located in Cambridge, MA. Prior to joining Pfizer, I was a Senior Investigator and Chief of the Immunopathogenesis Section of the Laboratory of Parasitic Disease, in the National Institute of Allergy and Infectious Diseases, NIH in Bethesda, MD. I received my Ph.D. from the Department of Medical Microbiology and Immunology at the University of Wisconsin, in Madison, Wisconsin. I have published over 200 research papers, reviews, and book chapters in many prestigious journals including Nature, Science, and Nature Immunology and have made important contributions to our understanding of the role of cytokines and growth factors in the progression and resolution of chronic inflammation, tissue regeneration, and fibrosis. At Pfizer, I’m leading our discovery efforts in the areas of immune tolerance, epithelial cell biology, immunometabolism, innate immunity, and fibrosis. For the past three years, I have been included on Thomson Reuters’ list of Highly Cited Researchers.
RESEARCH AREA(S)
The discovery group in the Inflammation and Immunology Research Unit focuses on core mechanisms that drive tissue damaging inflammation in important rheumatic, gastrointestinal, and dermatological diseases, including rheumatoid arthritis, systemic lupus erythematosus, ulcerative colitis, Crohn’s disease, non-alcoholic steatohepatitis, fibrosis, psoriasis, atopic dermatitis, alopecia, and vitiligo. Our work on immune tolerance is focused on identifying novel strategies to induce durable disease remission by harnessing endogenous regulatory mechanisms including immunosuppressive T cells. Epithelial cells have emerged as key drivers of several important chronic inflammatory diseases including atopic dermatitis, psoriasis, and IBD.
The epithelial biology group is using novel human cell based assays to better understand the role of the epithelium in disease pathogenesis and to test new therapeutics. The innate immunity is group is focused on understanding the role of danger sensing mechanisms and checkpoint (co-regulatory) receptor pathways in the initiation and maintenance of tissue damaging inflammatory responses. Similarly, the immunometabolism group is developing unique strategies to target metabolic pathways in important immune cells such as T cells and macrophages to restore immune homeostasis. Finally, the fibrosis groups is elucidating mechanisms that transform fat accumulation in the liver (steatosis) into a chronic inflammatory response (steatohepatitis) that can lead to fibrosis, cirrhosis, and ultimately organ failure that is rapidly becoming a leading cause of liver transplantation. A better understanding of the mechanisms that drive hepatic fibrosis could also reveal improved strategies to treat a variety of important fibrotic diseases including lupus nephritis, cardiovascular fibrosis, radiation induced fibrosis, and idiopathic pulmonary fibrosis.
PUBLICATIONS
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Type 2 immunity in tissue repair and fibrosis.
Nat Rev Immunol. 2018 Jan;18(1):62-76.
Gieseck RL 3rd, Wilson MS, Wynn TA.
https://www.ncbi.nlm.nih.gov/pubmed/28853443 -
Type 2 immunity is protective in metabolic disease but exacerbates NAFLD collaboratively with TGF-β.
Sci Transl Med. 2017 Jun 28;9(396).
Hart KM, Fabre T, Sciurba JC, Gieseck RL 3rd, Borthwick LA, Vannella KM, Acciani TH, de Queiroz Prado R, Thompson RW, White S, Soucy G, Bilodeau M, Ramalingam TR, Arron JR, Shoukry NH, Wynn TA.
https://www.ncbi.nlm.nih.gov/pubmed/28659437 -
Inflammation and metabolism in tissue repair and regeneration.
Science. 2017 Jun 9;356(6342):1026-1030.
Eming SA, Wynn TA, Martin P.
https://www.ncbi.nlm.nih.gov/pubmed/2859633 -
Interleukin-13 Activates Distinct Cellular Pathways Leading to Ductular Reaction, Steatosis, and Fibrosis.
Immunity. 2016 Jul 19;45(1):145-58.
Gieseck RL 3rd, Ramalingam TR, Hart KM, Vannella KM, Cantu DA, Lu WY, Ferreira-González S,
Forbes SJ, Vallier L, Wynn TA.
https://www.ncbi.nlm.nih.gov/pubmed/27421703 -
Combinatorial targeting of TSLP, IL-25, and IL-33 in type 2 cytokine-driven inflammation and fibrosis.
Sci Transl Med. 2016 May 4;8(337):337ra65.
Vannella KM, Ramalingam TR, Borthwick LA, Barron L, Hart KM, Thompson RW, Kindrachuk KN,
Cheever AW, White S, Budelsky AL, Comeau MR, Smith DE, Wynn TA.
https://www.ncbi.nlm.nih.gov/pubmed/27147589
EDUCATION
National Institutes of Health, Postdoctoral Fellow, 1995
University of Wisconsin – Madison, PhD, 1991
Miami University, B.A., 1986
AWARDS & HONORS
Thomson Reuters Highly Cited Researcher. 2014 – 2017
Elected to Fellowship in the American Academy of Microbiology, 2012
National Institutes of Health Merit Award, 2011
Bailey K. Ashford Medal, American Society of Tropical Medicine and Hygiene, 2006
Oswaldo Cruz Medal, Oswaldo Cruz Foundation, 2002
QUOTE
“I joined Pfizer so I could more effectively move basic science discoveries into the clinic so patient lives will be improved”
