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Todd N. Eagar, PhD

Assistant Professor of Pathology and Genomic Medicine, Institute for Academic Medicine
Assistant Research Member, Research Institute
Houston Methodist
Weill Cornell Medical College


Dr. Eagar received his PhD in immunology and molecular pathogenesis from the Northwestern University Medical School in Chicago in 2001. He then completed an immunology fellowship at the University of California at San Francisco and an HLA fellowship at Houston Methodist Hospital. Dr. Eagar was an assistant professor in the Department of Pathology and Immunology at The University of Texas Southwestern Medical Center in Dallas before joining the Department of Pathology and Genomic Medicine here in 2013.

Description of Research

Dr. Eagar is board certified in histocompatibility by the American Board of Histocompatibility and Immunogenetics. His research interests include identifying immune processes involved in the pathogenesis of multiple sclerosis and transplant rejection, with a focus on finding novel regulatory pathways involved in T cell activation that might be harnessed for therapeutic intervention.


A single amino acid substitution prevents recognition of a dominant human aquaporin-4 determinant in the context of HLA-DRB1-03: 01 by a murine TCR
Arellano, B, Hussain, R, Miller-Little, WA, Herndon, E, Lambracht-Washington, D, Eagar, TN, Lewis, R, Healey, D, Vernino, S, Greenberg, BM & Stüve, O 2016, PLoS ONE, vol 11, no. 4, e0152720. DOI:

T cell subsets and their signature cytokines in autoimmune and inflammatory diseases
Raphael, I, Nalawade, S, Eagar, TN & Forsthuber, TG 2015, Cytokine, vol 74, no. 1, pp. 5-17. DOI:

Immune surveillance of the central nervous system in multiple sclerosis - Relevance for therapy and experimental models
Hussain, RZ, Hayardeny, L, Cravens, PC, Yarovinsky, F, Eagar, TN, Arellano, B, Deason, K, Castro-Rojas, C & Stüve, O 2014, Journal of Neuroimmunology, vol 276, no. 1-2, pp. 9-17. DOI:

Testing effects of glatiramer acetate and fingolimod in an infectious model of CNS immune surveillance
Castro-Rojas, C, Deason, K, Hussain, RZ, Hayardeny, L, Cravens, PC, Yarovinsky, F, Eagar, TN, Arellano, B & Stüve, O 2014, Journal of Neuroimmunology, vol 276, no. 1-2, pp. 232-235. DOI:

A peptide prime-DNA boost immunization protocol provides significant benefits as a new generation Aß42 DNA vaccine for Alzheimer disease
Lambracht-Washington, D, Qu, BX, Fu, M, Anderson, LD, Eagar, TN, Stüve, O & Rosenberg, RN 2013, Journal of Neuroimmunology, vol 254, no. 1-2, pp. 63-68. DOI:

Helper T-cell subsets and control of the inflammatory response
Eagar, TN & Miller, SD 2012, . in Clinical Immunology: Principles and Practice: Fourth Edition. Elsevier Inc. pp. 203-214. DOI:

Parkinson's disease: A role for the immune system
German, DC, Eagar, T & Sonsalla, PK 2012, Current Molecular Pharmacology, vol 5, no. 3, pp. 340-349. DOI:

DNA immunization against amyloid beta 42 has high potential as safe therapy for Alzheimer's disease as it diminishes antigen-specific Th1 and Th17 cell proliferation.
Lambracht-Washington, D, Qu, BX, Fu, M, Anderson, LD, Stüve, O, Eagar, TN & Rosenberg, RN 2011, Cellular and Molecular Neurobiology, vol 31, no. 6, pp. 867-874.

Lymph node-derived donor encephalitogenic CD4+ T cells in C57BL/6 mice adoptive transfer experimental autoimmune encephalomyelitis highly express GM-CSF and T-bet
Cravens, PD, Hussain, RZ, Zacharias, TE, Ben, LH, Herndon, E, Vinnakota, R, Lambracht-Washington, D, Nessler, S, Zamvil, SS, Eagar, TN & Stüve, O 2011, Journal of Neuroinflammation, vol 8, 73. DOI:

DNA Immunization Against Amyloid beta 42 has High Potential as Safe Therapy for Alzheimer's Disease as it Diminishes Antigen-Specific Th1 and Th17 Cell Proliferation
Lambracht-Washington, D, Qu, BX, Fu, M, Anderson, LD, Stüve, O, Eagar, TN & Rosenberg, RN 2011, Cellular and Molecular Neurobiology, pp. 1-8. DOI:

Rituximab therapy reduces organ-specific T cell responses and ameliorates experimental autoimmune encephalomyelitis
Monson, NL, Cravens, P, Hussain, R, Harp, CT, Cummings, M, Martin, MDP, Ben, LH, Do, J, Lyons, JA, Lovette-Racke, A, Cross, AH, Racke, MK, Stüve, O, Shlomchik, M & Eagar, TN 2011, PLoS ONE, vol 6, no. 2, e17103. DOI:

Translational research in neurology and neuroscience 2010: Multiple sclerosis
Stüve, O, Kieseier, BC, Hemmer, B, Hartung, HP, Awad, A, Frohman, EM, Greenberg, BM, Racke, MK, Zamvil, SS, Phillips, JT, Gold, R, Chan, A, Zettl, U, Milo, R, Marder, E, Khan, O & Eagar, TN 2010, Archives of Neurology, vol 67, no. 11, pp. 1307-1315. DOI:

Memory B cells from a subset of treatment-naïve relapsing-remitting multiple sclerosis patients elicit CD4+ T-cell proliferation and IFN-? production in response to myelin basic protein and myelin oligodendrocyte glycoprotein
Harp, CT, Ireland, S, Davis, LS, Remington, G, Cassidy, B, Cravens, PD, Stuve, O, Lovett-Racke, AE, Eagar, TN, Greenberg, BM, Racke, MK, Cowell, LG, Karandikar, NJ, Frohman, EM & Monson, NL 2010, European Journal of Immunology, vol 40, no. 10, pp. 2942-2956. DOI:

Analysis of three plasmid systems for use in DNA Aß42 immunization as therapy for Alzheimer's disease
Qu, BX, Lambracht-Washington, D, Fu, M, Eagar, TN, Stüve, O & Rosenberg, RN 2010, Vaccine, vol 28, no. 32, pp. 5280-5287. DOI:

Pharmacological prion protein silencing accelerates central nervous system autoimmune disease via T cell receptor signalling
Hu, W, Nessler, S, Hemmer, B, Eagar, TN, Kane, LP, Leliveld, SR, Müller-Schiffmann, A, Gocke, AR, Lovett-Racke, A, Ben, LH, Hussain, RZ, Breil, A, Elliott, JL, Puttaparthi, K, Cravens, PD, Singh, MP, Petsch, B, Stitz, L, Racke, MK, Korth, C & Stüve, O 2010, Brain, vol 133, no. 2, pp. 375-388. DOI:

Reversible alopecia associated with glatiramer acetate
Pacheco, MF, Jacobe, H, Eagar, TN & Stüve, O 2010, Archives of Neurology, vol 67, no. 9, pp. 1154.

Direct and consensual murine pupillary reflex metrics: Establishing normative values
Hussain, RZ, Hopkins, SC, Frohman, EM, Eagar, TN, Cravens, PC, Greenberg, BM, Vernino, S & Stüve, O 2009, Autonomic Neuroscience: Basic and Clinical, vol 151, no. 2, pp. 164-167. DOI:

Interactions between PD-1 and PD-L1 promote tolerance by blocking the TCR-induced stop signal.
Fife, BT, Pauken, KE, Eagar, TN, Obu, T, Wu, J, Tang, Q, Azuma, M, Krummel, MF & Bluestone, JA 2009, Nature Immunology, vol 10, no. 11, pp. 1185-1192. DOI:

Depletion of B lymphocytes from cerebral perivascular spaces by rituximab
Martin, MDP, Cravens, PD, Winger, R, Kieseier, BC, Cepok, S, Eagar, TN, Zamvil, SS, Weber, MS, Frohman, EM, Kleinschmidt-DeMasters, BK, Montine, TJ, Hemmer, B, Marra, CM & Stüve, O 2009, Archives of Neurology, vol 66, no. 8, pp. 1016-1020. DOI:

200 years after darwin
Rosenberg, RN, Stüve, O & Eagar, T 2009, JAMA - Journal of the American Medical Association, vol 301, no. 6, pp. 660-662. DOI: