Jennifer Gommerman | |
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Born | Winnipeg, Manitoba |
Academic background | |
Education | BSc, 1993, PhD, immunology, 1998, University of Toronto |
Thesis | An analysis of steel factor-stimulated receptor trafficking, survival signals and mitogenesis: understanding the role of c-Kit-associated signaling proteins (2000) |
Academic work | |
Institutions | University of Toronto |
Jennifer Lynn Gommerman is a Canadian immunologist. She is a Tier 1 Canada Research Chair in Tissue-Specific Immunity at the University of Toronto. Gommerman has been examining the role of B lymphocytes in Multiple Sclerosis patients and in animal models of MS. She also studies the antibody response to SARS-CoV-2 in saliva samples from patients with COVID-19. [1]
Gommerman was born in Winnipeg,Manitoba but her family moved to Burlington,Ontario when she was 10 years old. Growing up in Burlington,she attended Ecole St. Philippe and then Lester B. Pearson High School before enrolling at the University of Toronto (U of T). [2] She subsequently earned her Bachelor of Science degree and Ph.D. in immunology at U of T [3] before completing a post-doctoral fellowship at Harvard Medical School. [2]
Following her post-doctoral fellowship,Gommerman became a staff scientist at Biogen Inc for three years before returning to U of T in 2003 as an assistant professor of immunology. [2] She intended to continue her work with multiple sclerosis (MS) but eventually broadened her research to include the impact of the mucosal immune system in the gut on diseases such as MS. [4] In 2007,Gommerman received an Early Researcher Award to support her efforts in uncovering the basic set of biological events common to MS and other chronic diseases. [5] In 2014,Gommerman began investigating chronic inflammatory diseases in South Asian immigrants raised in Canada using funding from the Global Challenge Prize. Her research project was entitled the GEMINI Study (Generational differences in Environmental exposures caused by Human Migration:Impact on Incidence of Inflammatory Disease). [6] At the same time,she also assumed the role of graduate coordinator and was promoted to the rank of full professor. [2]
As a full professor,Gommerman continued examining the role of B lymphocytes in Multiple Sclerosis patients. In 2019,in collaborating with researchers at UC San Francisco,Gommerman discovered that the intestine is the source of immune cells that reduce brain inflammation in people with multiple sclerosis. As such,increasing the number of these cells blocks inflammation entirely in a preclinical model of the disease. [7] She also began using non-traditional methods to detect dozens of proteins in a single tissue section. She used imaging mass cytometry to study the immune cells found in brain lesions of MS patients. [8] In 2020,Gommerman and her post-doctoral researcher Conglei Li discovered that in utero inhibition of molecular signalling in the guts of mice can compromise immunity in adulthood. This early disruption limits the ability of the immune system to later trigger and generate Immunoglobulin A (IgA) antibodies. It also interferes with the nature and function of cells in the gut that support the antibody response. [9]
Early in the COVID-19 pandemic,Gommerman helped with developing a blood test to identify who is immune to the novel virus on a mass scale. She helped supply samples from pre-pandemic subjects as well as patients infected early in the pandemic who have since recovered. [10] She was also appointed a Tier 1 Canada Research Chair in Tissue-Specific Immunity at U of T. [11] She continued to lead saliva testing efforts in this new role and worked with a research team which found that coronavirus antibodies could last at least three months after a person becomes infected with the virus. [12] She also helped organize and lead the Coronavirus Variants Rapid Response Network for research on COVID-19 variants. [13] Beyond COVID-19,Gommerman continued her research into MS and used funding from the Multiple Sclerosis Society of Canada to investigate on the interplay between the complement system and glial cells in the hippocampus. The purpose of this project was to determine the changes that occur in the brains of people with progressive MS and how it correlates with clinical disability. [8]
In immunology,autoimmunity is the system of immune responses of an organism against its own healthy cells,tissues and other normal body constituents. Any disease resulting from this type of immune response is termed an "autoimmune disease". Prominent examples include celiac disease,post-infectious IBS,diabetes mellitus type 1,Henoch–Schönlein purpura (HSP) sarcoidosis,systemic lupus erythematosus (SLE),Sjögren syndrome,eosinophilic granulomatosis with polyangiitis,Hashimoto's thyroiditis,Graves' disease,idiopathic thrombocytopenic purpura,Addison's disease,rheumatoid arthritis (RA),ankylosing spondylitis,polymyositis (PM),dermatomyositis (DM),and multiple sclerosis (MS). Autoimmune diseases are very often treated with steroids.
Immunodeficiency,also known as immunocompromisation,is a state in which the immune system's ability to fight infectious diseases and cancer is compromised or entirely absent. Most cases are acquired ("secondary") due to extrinsic factors that affect the patient's immune system. Examples of these extrinsic factors include HIV infection and environmental factors,such as nutrition. Immunocompromisation may also be due to genetic diseases/flaws such as SCID.
A demyelinating disease is any disease of the nervous system in which the myelin sheath of neurons is damaged. This damage impairs the conduction of signals in the affected nerves. In turn,the reduction in conduction ability causes deficiency in sensation,movement,cognition,or other functions depending on which nerves are involved.
Rituximab,sold under the brand name Rituxan among others,is a monoclonal antibody medication used to treat certain autoimmune diseases and types of cancer. It is used for non-Hodgkin lymphoma,chronic lymphocytic leukemia,rheumatoid arthritis,granulomatosis with polyangiitis,idiopathic thrombocytopenic purpura,pemphigus vulgaris,myasthenia gravis and Epstein–Barr virus-positive mucocutaneous ulcers. It is given by slow injection into a vein. Biosimilars of Rituxan include Blitzima,Riabni,Ritemvia,Rituenza,Rixathon,Ruxience,and Truxima.
Natalizumab,sold under the brand name Tysabri among others,is a medication used to treat multiple sclerosis and Crohn's disease. It is a humanized monoclonal antibody against the cell adhesion molecule α4-integrin. It is given by intravenous infusion every 28 days. The drug is believed to work by reducing the ability of inflammatory immune cells to attach to and pass through the cell layers lining the intestines and blood–brain barrier. Natalizumab has proven effective in treating the symptoms of both diseases,preventing relapse,vision loss,cognitive decline and significantly improving quality of life in people with multiple sclerosis,as well as increasing rates of remission and preventing relapse in multiple sclerosis.
Helminthic therapy,an experimental type of immunotherapy,is the treatment of autoimmune diseases and immune disorders by means of deliberate infestation with a helminth or with the eggs of a helminth. Helminths are parasitic worms such as hookworms,whipworms,and threadworms that have evolved to live within a host organism on which they rely for nutrients. These worms are members of two phyla:nematodes,which are primarily used in human helminthic therapy,and flat worms (trematodes).
Experimental autoimmune encephalomyelitis,sometimes experimental allergic encephalomyelitis (EAE),is an animal model of brain inflammation. It is an inflammatory demyelinating disease of the central nervous system (CNS). It is mostly used with rodents and is widely studied as an animal model of the human CNS demyelinating diseases,including multiple sclerosis (MS) and acute disseminated encephalomyelitis (ADEM). EAE is also the prototype for T-cell-mediated autoimmune disease in general.
Multiple sclerosis is an inflammatory demyelinating disease of the CNS in which activated immune cells invade the central nervous system and cause inflammation,neurodegeneration,and tissue damage. The underlying cause is currently unknown. Current research in neuropathology,neuroimmunology,neurobiology,and neuroimaging,together with clinical neurology,provide support for the notion that MS is not a single disease but rather a spectrum.
Multiple sclerosis and other demyelinating diseases of the central nervous system (CNS) produce lesions and glial scars or scleroses. They present different shapes and histological findings according to the underlying condition that produces them.
A TNF inhibitor is a pharmaceutical drug that suppresses the physiologic response to tumor necrosis factor (TNF),which is part of the inflammatory response. TNF is involved in autoimmune and immune-mediated disorders such as rheumatoid arthritis,ankylosing spondylitis,inflammatory bowel disease,psoriasis,hidradenitis suppurativa and refractory asthma,so TNF inhibitors may be used in their treatment. The important side effects of TNF inhibitors include lymphomas,infections,congestive heart failure,demyelinating disease,a lupus-like syndrome,induction of auto-antibodies,injection site reactions,and systemic side effects.
Inflammatory demyelinating diseases (IDDs),sometimes called Idiopathic (IIDDs) due to the unknown etiology of some of them,are a heterogenous group of demyelinating diseases - conditions that cause damage to myelin,the protective sheath of nerve fibers - that occur against the background of an acute or chronic inflammatory process. IDDs share characteristics with and are often grouped together under Multiple Sclerosis. They are sometimes considered different diseases from Multiple Sclerosis,but considered by others to form a spectrum differing only in terms of chronicity,severity,and clinical course.
Chronic systemic inflammation (SI) is the result of release of pro-inflammatory cytokines from immune-related cells and the chronic activation of the innate immune system. It can contribute to the development or progression of certain conditions such as cardiovascular disease,cancer,diabetes mellitus,chronic kidney disease,non-alcoholic fatty liver disease,autoimmune and neurodegenerative disorders,and coronary heart disease.
Interleukin-17A is a protein that in humans is encoded by the IL17A gene. In rodents,IL-17A used to be referred to as CTLA8,after the similarity with a viral gene.
An autoimmune disease is a condition arising from an abnormal immune response to a functioning body part. At least 80 types of autoimmune diseases have been identified,with some evidence suggesting that there may be more than 100 types. Nearly any body part can be involved. Common symptoms can be diverse and transient,ranging from mild to severe,and generally include low grade fever and feeling tired.
Immunoglobulin therapy is the use of a mixture of antibodies to treat several health conditions. These conditions include primary immunodeficiency,immune thrombocytopenic purpura,chronic inflammatory demyelinating polyneuropathy,Kawasaki disease,certain cases of HIV/AIDS and measles,Guillain-Barrésyndrome,and certain other infections when a more specific immunoglobulin is not available. Depending on the formulation it can be given by injection into muscle,a vein,or under the skin. The effects last a few weeks.
Type 3 innate lymphoid cells (ILC3) are immune cells from the lymphoid lineage that are part of the innate immune system. These cells participate in innate mechanisms on mucous membranes,contributing to tissue homeostasis,host-commensal mutualism and pathogen clearance. They are part of a heterogeneous group of innate lymphoid cells,which is traditionally divided into three subsets based on their expression of master transcription factors as well as secreted effector cytokines - ILC1,ILC2 and ILC3.
Otilimab is a fully human antibody which has been developed by the biotechnology company MorphoSys. It can also be referred to as HuCAL antibody,HuCAL standing for Human Combinatorial Antibody Library and being a technology used to generate monoclonal antibodies. Otilimab is directed against the granulocyte-macrophage colony stimulating factor (GM-CSF),a monomeric glycoprotein functioning as a cytokine promoting both proliferation and activation of macrophages and neutrophils.
Tania H. Watts is a Canadian Immunologist,Professor at the University of Toronto,past President of the Canadian Society for Immunology and from 2009-2019 held the Sanofi Pasteur Chair in Human Immunology at the University of Toronto. Tania Watts holds a Tier 1 Canada Research Chair in Anti-viral Immunity and was named a Distinguished Fellow of the American Association of Immunologists,class of 2022.
Anne Cross is an American neurologist and neuroimmunologist and the Section Head of Neuroimmunology at Washington University School of Medicine in St. Louis,Missouri. Cross holds the Manny and Rosalyn Rosenthal–Dr. John L. Trotter Endowed Chair in Neuroimmunology at WUSTL School of Medicine and co-directs the John L Trotter Multiple Sclerosis Clinic at Barnes-Jewish Hospital. Cross is a leader in the field of neuroimmunology and was the first to discover the role of B cells in the pathogenesis of multiple sclerosis in animals and then in humans. Cross now develops novel imaging techniques to observe inflammation and demyelination in the central nervous systems of MS patients for diagnosis and disease management.
Burkhard Becher is a German immunologist,biomedical researcher and academic. He is a Professor and Chair of the Institute of Experimental Immunology at the University of Zurich.