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Irah King

Assistant Professor

Department of Microbiology and Immunology

Duff Medical Building - Room 406
3775 University Street
Montreal, QC H3A 2B4

Tel: (514) 398-7325
Lab: (514) 398-7528
Fax: (514) 398-7052
Lab website: http://www.ikinglab.com


Research description

The ability to generate robust and specific antibodies to diverse infectious agents is a fundamental property of the adaptive immune system that is critical for host survival. This response, termed humoral immunity, requires highly coordinated interactions within the secondary lymphoid organs between B lymphocytes (which possess antibody-producing potential) and “helper” T cells. Only recently has it become clear that a particular subset of these helper T cells possess the unique ability to enter the B cell follicles of the lymphoid organs and provide direct help to B cells through provision of membrane-bound co-stimulatory molecules and secretion of B cell-polarizing cytokines. As a result, this T cell subset has been aptly named T follicular helper (Tfh) cells. My previous work has identified novel subsets of innate and adaptive T cells capable of providing help to B cells through provision of both cognate and soluble factors. Most notably, I found Tfh cells to be the dominant interleukin (IL)-4 producing cell in the reactive lymph node of helminth-infected mice, a model of Th2-driven immunity. Given the established importance of IL-4 in both humoral immunity to infection and Th2-driven diseases such as allergy and asthma, this setting of infection provides an ideal platform to investigate fundamental mechanisms of Tfh as well as Th2 cell differentiation. Although significant progress has recently been made in the study of Th2 and Tfh cell biology, fundamental questions remain with particular regard to their requirements for differentiation and persistence in the context of diverse settings of infection and immunity. The overall goals of my research program are to 1) identify the cellular and molecular requirements for Tfh and Th2 cell differentiation, 2) how they function to generate protective humoral immunity to infection and 3) determine the mechanisms by Tfh cells localize and persist in the germinal center niche during chronic infection.


Selected Publications

Amiel E, Everts B, Freitas TC, King IL, Curtis JD, Pearce EL, Pearce EJ. Inhibition of mTOR promotes dendritic cell activation and enhances therapeutic autologous vaccination in mice. Journal of Immunology. 2012 Sept. 1.

Fairfax KC, Amiel E, King IL, Freitas TC, Mohrs M, Pearce EJ. IL-10R blockade during chronic Schistosoma mansoni infection results in the loss of B cells from the liver and the development of severe pulmonary disease. PLOS Pathogens. 2012 8(1): e1002490.

King IL, Fortier A, Tighe M, Dibble J, Watts G, Veerapen N, Haberman A, Besra G, Mohrs M, Brenner MB, Leadbetter EA. Invariant natural killer T cells direct B cell responses to cognate lipid antigen in an IL-21-dependent manner. Nature Immunology. 2012 Jan;13(1):44-50.

Lu SM, Tremblay MÈ, King IL, Qi JL, Reynolds HM, Marker DF, Varrone JJ, Majewska AK, Dewhurst S, Gelbard HA. HIV-1 Tat-Induced Microgliosis and Synaptic Damage via Interactions between Peripheral and Central Myeloid Cells. PLoS One. 2011;6(9):e23915.

King IL, Mohrs K, Mohrs M. A Non-Redundant Role for IL-21 Receptor Signaling in Plasma Cell Differentiation and Protective Type 2 Immunity Against Gastrointestinal Helminth Infection. Journal of Immunology. 2010 Nov 15;185(10):6138-45.

King IL, Kroenke MA and Segal BM. GM-CSF dependent, CD103+ dermal dendritic cells play a critical role in Th effector differentiation following subcutaneous immunization. Journal of Experimental Medicine.  2010 May 10;207(5):953-61.

King IL and Mohrs M. IL-4 producing Th2 cells in the reactive lymph node during helminth infection are T follicular helper cells. Journal of Experimental Medicine. 2009 May 11;206(5):1001-7.

Zaretsky AG, Taylor JT, King IL, Marshall F, Mohrs M and Pearce EJ. T follicular helper cells differentiate from Th2 cells in a B cell dependent manner in response to helminth antigens. Journal of Experimental Medicine. 2009 May 11;206(5):991-9.  

King IL, Dickendesher TL and Segal BM. Circulating Ly-6C+ myeloid precursors migrate to the CNS and play a pathogenic role during autoimmune demyelinating disease. Blood. 2009 Apr 2;113(14):3190-7.

Deshpande P, King IL and Segal BM. Cutting Edge: CNS CD11c+ cells from mice with encephalomyelitis polarize Th17 cells and support CD25+CD4+ mediated immunosuppression, suggesting dual roles in the disease process. J Immunology. 2007 Jun 1;178(11):6695-9.

Deshpande P, King IL and Segal BM. IL-12 driven upregulation of P-selectin ligand on myelin-specific T cells is a critical step in an animal model of autoimmune demyelination. J Neuroimmunology. 2006 Apr;173(1-2):35-44.

King IL and Segal BM. Cutting edge: IL-12 induces CD4+CD25- T cell activation in the presence of T regulatory cells. J Immunology. 2005 Jul 15;175(2):641-5.


Publications - Irah King