Jennifer Gommerman

See our recent work in collaboration with the lab of Drs. Anne-Claude Gingras and Allison McGeer on antibodies to SARS-CoV-2 in saliva and blood

Science Immunology  08 Oct 2020: Vol. 5, Issue 52 (DOI: 10.1126/sciimmunol.abe5511

Our Lab

Autoimmune diseases such as Multiple Sclerosis (MS) pose an enormous burden on our Canadian society. For reasons that are unclear, such diseases are on the rise. Moreover, therapies for these diseases remain relatively non-specific, targeting large arms of the immune system. Some forms of autoimmunity, such as progressive MS, have no effective treatments. My lab is focused on (1) mechanisms of immune dysregulation in autoimmune disease, particularly MS; (2) understanding the reason for the rapid increase in autoimmune disease observed in Canada and (3) determining the role of TNF family members in immune cell biology.

We enjoy the benefits of a collaborative team representing a diverse skill ideal for study of human and mouse model systems. Our weekly lab meetings and journal clubs, as well as social outings such as an annual canoe trip, facilitate effective team-work and an enjoyable work atmosphere.

Dr. Gommerman is a Canada Research Chair in Tissue Specific Immunity.

Research Synopsis

Dysregulation of immune cell function in autoimmunity

MS is a complex disease with no known cause or cure. Based on genetic and pathology data, we know that the immune system plays a very important role in this disease. My lab is interested in how immune cells become activated with the CNS environment. In particular, using an animal model of MS (Experimental Autoimmune Encephalomyelitis), we have been studying immune cell rich structures found in the meninges. In addition, Immunologists have learned that B-lymphocytes play a very important role in modulating autoimmunity. In collaboration with a multi-disciplinary team of neuroimmunologists and using a number of animal and human model systems, we are currently exploring how pro- and anti- inflammatory B cells impact MS pathogenesis. Lastly, we are particularly interested in how the mucosal immune system in the gut influences autoimmune responses in the CNS. This work is supported by the MS Society of Canada (single PI grant) and the MS Society Research Foundation of Canada (team grant with Drs. Amit Bar-Or and Alexandre Prat).

Why are autoimmune disease on the rise in Canada?

The highest prevalence of chronic inflammatory diseases is found in northern latitude countries where a 3- 5-fold incidence increase has been observed over the last 30-50 years. Such a rapid rise in disease can only be explained by environmental changes, the nature of which remains unknown. We have focused on the gut microbiome as a possible modifier of disease risk in genetically susceptible individuals. The gut microbiome is one of the most densely populated bacterial communities, and, in the gut, interactions between the microbiome and the host immune system are played out across a thin barrier comprised of epithelial cells. Using a combination of animal models and human tissues, we are examining interactions between the microbiome and the mucosal immune system, in particular mucosal B lineage cells such as IgA+ plasma cells. We are exploring how this large reservoir of IgA+ plasma cells reflects ongoing responses to the microbiome and what role IgA+ plasma cells may play in inflammatory responses. This work is supported by Canadian Institutes of Health Research Research (single PI grant) and the Connaught Foundation (team grant, JG as principal PI).

TNF family members and immune cell biology

TNF family members play diverse roles in the immune system, and therapies for treatment of some autoimmune disease are targeted at TNF family members. We have a long-standing interest in both the Lymphtooxin and BAFF pathways in the context of chronic inflammatory conditions. Using a combination of animal models and human systems, we are interrogating the role of these pathways in a variety of immune contexts including mucosal IgA responses, germinal centre reactions and Dendritic Cell biology. This work is supported by Canadian Institutes of Health Research Research (single PI grant) and the Kidney Foundation (single PI grant). 

Recent Publications

Sr or co-Sr Author data papers, Last 7 Years:

• Recirculating Intestinal IgA-Producing Cells Regulate Neuroinflammation via IL-10. Rojas OL, Pröbstel AK, Porfilio EA, Wang AA, Charabati M, Sun T, Lee DSW, Galicia G, Ramaglia V, Ward LA, Leung LYT, Najafi G, Khaleghi K, Garcillán B, Li A, Besla R, Naouar I, Cao EY, Chiaranunt P, Burrows K, Robinson HG, Allanach JR, Yam J, Luck H, Campbell DJ, Allman D, Brooks DG, Tomura M, Baumann R, Zamvil SS, Bar-Or A, Horwitz MS, Winer DA, Mortha A, Mackay F, Prat A, Osborne LC, Robbins C, Baranzini SE, Gommerman JL.  Cell. 2019 Jan 24;176(3):610-624.
• Isotype-Switched Autoantibodies Are Necessary To Facilitate Central Nervous System Autoimmune Disease in Aicda-/- and Ung-/- Mice. Galicia G, Lee DSW, Ramaglia V, Ward LA, Yam JY, Leung LYT, Li R, Handy M, Zhang J, Drohomyrecky PC, Lancaster E, Bar-Or A, Martin A, Gommerman JL. J Immunol. 2018 Aug 15;201(4):1119-1130. doi: 10.4049/jimmunol.1700729. Epub 2018 Jul 6.
• Intestinal Batf3-dependent dendritic cells are required for optimal antiviral T-cell responses in adult and neonatal mice. Sun T, Rojas OL, Li C, Ward LA, Philpott DJ, Gommerman JL. Mucosal Immunol. 2017 May;10(3):775-788
• Integration of Th17- and Lymphotoxin-Derived Signals Initiates Meningeal-Resident Stromal Cell Remodeling to Propagate Neuroinflammation. Pikor NB, Astarita JL, Summers-Deluca L, Galicia G, Qu J, Ward LA, Armstrong S, Dominguez CX, Malhotra D, Heiden B, Kay R, Castanov V, Touil H, Boon L, O'Connor P, Bar-Or A, Prat A, Ramaglia V, Ludwin S, Turley SJ, Gommerman JL.
• Hematopoietic LTβR deficiency results in skewed T cell cytokine profiles during a mucosal viral infection. Sun T, Rojas OL, Li C, Philpott DJ, Gommerman JL. J Leukoc Biol. 2016 Jul;100(1):103-10. doi: 10.1189/jlb.4MAB0715-294R. Epub 2015 Dec 10.
• A Lymphotoxin/Type I IFN Axis Programs CD8+ T Cells To Infiltrate a Self-Tissue and Propagate Immunopathology. Ng D, Maître B, Cummings D, Lin A, Ward LA, Rahbar R, Mossman KL, Ohashi PS, Gommerman JL. J Immunol. 2015 Nov 15;195(10):4650-9. 
• AID and caspase 8 shape the germinal center response through apoptosis.Boulianne B, Rojas OL, Haddad D, Zaheen A, Kapelnikov A, Nguyen T, Li C, Hakem R, Gommerman JL, Martin A.J Immunol. 2013 Dec 15;191(12):5840-7. 
• AID-expressing germinal center B cells cluster normally within lymph node follicles in the absence of FDC-M1+ CD35+ follicular dendritic cells but dissipate prematurely. Boulianne B, Le MX, Ward LA, Meng L, Haddad D, Li C, Martin A, Gommerman JL. J Immunol. 2013 Nov 1;191(9):4521-30. 
• Secondary B cell receptor diversification is necessary for T cell mediated neuro-inflammation during experimental autoimmune encephalomyelitis. Galicia G, Boulianne B, Pikor N, Martin A, Gommerman JL. PLoS One. 2013 Apr 22;8(4)
• A sphingosine-1-phosphate receptor 1-directed agonist reduces central nervous system inflammation in a plasmacytoid dendritic cell-dependent manner. Galicia-Rosas G, Pikor N, Schwartz JA, Rojas O, Jian A, Summers-Deluca L, Ostrowski M, Nuesslein-Hildesheim B, Gommerman JL. J Immunol. 2012 Oct 1;189(7):3700-6. 
• Acquisition of a multifunctional IgA+ plasma cell phenotype in the gut. Fritz JH, Rojas OL, Simard N, McCarthy DD, Hapfelmeier S, Rubino S, Robertson SJ, Larijani M, Gosselin J, Ivanov II, Martin A, Casellas R, Philpott DJ, Girardin SE, McCoy KD, Macpherson AJ, Paige CJ, Gommerman JL. Nature. 2011 Dec 11;481(7380):199-203.

Appointments

Canada Research Chair in Tissue Specific Immunity