Thomas Edward Lane

picture of Thomas Edward Lane

Chancellor's Professor, Neurobiology and Behavior
School of Biological Sciences

Director, Center for Virus Research

Ph.D., UCLA School of Medicine, 1993, Microbiology & Immunology

Phone: (949) 824-1360

University of California, Irvine
2205 McGaugh Hall, Room 2213
Mail Code: 4550
Irvine, CA 92697
Research Interests
Neuroinflammation, Neuroimmunology, Neurodegeneration, Murine Coronavirus, SARS-CoV2, Pathogenesis
Academic Distinctions
Chancellor's Professor, UC Irvine
Organizer, FASEB: Translational Neuroimmunology: From Mechanisms to Therapeutics, Virtual Conference - 2018 & 2020
Chancellor’s Fellow, UC Irvine
Associate Director, Institute of Immunology, UC Irvine
Director, Multiple Sclerosis Research Center, UC Irvine
Director, University of California, Irvine, Master’s Program in Biotechnology
Scripps Research Institute 1994-1997
Research Abstract
Work in my laboratory is divided into two main research areas: 1) define the functional contributions of chemokines and chemokine receptors in defense and disease following viral infection of the central nervous system (CNS) and 2) evaluate the therapeutic potential of mouse/human neural precursor cells (NPCs) in clinical recovery and remyelination in a model of viral-induced demyelination. My laboratory has a long-standing interest in understanding events that initiate and maintain inflammation within the CNS in response to viral infection. To this end, we have set forth on a directed path to determine the functional significance of chemokines and chemokine receptors in both host defense as well as disease development following instillation of a positive-strand RNA virus (mouse hepatitis virus – MHV) into the CNS of susceptible mice. Indeed, we have shown that blocking chemokine function via both antibody neutralization and genetic silencing in virally-infected mice resulted in increased mortality accompanied by reduced immune cell infiltration into the CNS. Subsequently, we have demonstrated that unique chemokine/chemokine receptor signaling pathways are critical for interrelated events required for optimal host defense following viral infection including linking innate and adaptive immune responses, regulating antiviral effector functions e.g. cytokine secretion/cytolytic activity by effector T cells, and promoting the directional migration of antigen-sensitized lymphocytes into the CNS. We have also focused on how chemokine signaling influences the biology of oligodendroglia with regards to protection from inflammatory cytokine-induced apoptosis.

Similar to the human demyelinating disease multiple sclerosis (MS), remyelination failure is also observed in MHV-infected mice. Therefore, an important and clinically-relevant question related to demyelinating diseases is to design therapies that promote remyelination of demyelinated axons. We have determined that surgical engraftment of mouse neural precursosr cells (NPCs) into mice persistently-infected with MHV results in survival and migration of engrafted NPCs accompanied by extensive remyelination. The use of a viral model of demyelination is relevant in that the etiology of MS remains enigmatic and viruses have long been considered important as a potential triggering agent in inducing demyelinating diseases. Moreover, numerous viruses are capable of persisting within the CNS therefore understanding if NPCs are capable of promoting repair within an environment in which a persistent virus is present resulting in chronic neuroinflammation/demyelination is critical. We have determined that transplanted cells migrate to areas of demyelination by responding to the specific chemokines expressed within areas of demyelination. We have now moved forward with our studies on NPC-mediated clinical/histological recovery to address whether allogeneic NPCs are antigenic and subject to immune-mediated rejection. We are also investigating the therapeutic potential of human NPCs (hNPCs) in mediating functional recovery following transplantation into MHV-infected mice.

In response to the COVID19 pandemic, we are now exploring the ability of SARS-CoV2 to enter and replicate within the CNS. More specifically, we are employing human brain organoids as well as human iPSC-derived microglia, astrocytes and neurons to assess the ability of SARS-CoV2 to infect and replicate in these cells, induce cytopathology, and evaluate innate immune responses. In addition, we are using pre-clinical animal models to evaluate the ability of SARS-CoV2 to enter CNS following intranasal inoculation, identify target cells infected, and identify molecular and cellular mechanisms by which the immune system contributes to controlling replication. We are also testing novel anti-viral drugs for the ability to impede viral replication both in vitro and in vivo.
Awards and Honors
Research Volunteer of the Year Award, Pacific Coast MS Chapter
John Weiss Award for Excellence in Experimental Pathology, Department of Pathology, University of Utah
International Society for Neurovirology Audrey Steinman Gilden Lectureship
Elected AAAS Fellow, 2020
Short Biography
Tom Lane has been working in evaluating mechanisms governing neuroinflammation in response to infection, injury, or autoimmune-induced neurologic disease. After completing his Ph.D. research in Microbiology and Immunology at the UCLA School of Medicine, he did his postdoctoral work in neurovirology at the Scripps Research Institute in La Jolla, CA. Dr. Lane joined the Biological Sciences faculty at UC Irvine in 1998 where he is now a Chancellor’s Professor of Neurobiology & Behavior. Dr. Lane has served as Director of the Multiple Sclerosis (MS) Research Center and Associate Director of the Institute for Immunology. Dr. Lane was awarded a National Multiple Sclerosis Society (NMSS) Collaborative Center Award as well as a California Institute for Regenerative Medicine (CIRM) Early Translation Award dedicated to exploring the therapeutic potential of neural stem cells in treating human demyelinating diseases with a primary focus on MS.

Another area of ongoing work in the Lane laboratory is to define mechanisms associated with host defense and disease following infection of the central nervous system (CNS) with neuroadapted strains of murine coronaviruses (MuCoV) which induces an acute encephalomyelitis followed by a chronic immune-mediated demyelinating disease that has similar clinical and histologic disease to MS. More recently, Dr. Lane’s laboratory is exploring how infection of susceptible transgenic mice expressing the human angiotensin converting enzyme 2 (hACE2) which is the receptor for SARS-CoV-2 which is the causative agent for COVID-19. We are currently exploring mechanisms by which SARS-CoV-2 infection leads to neurologic disease by either directly infecting the CNS or through induction of an acute cytokine/chemokine storm. Furthermore, there is ongoing testing of anti-viral drugs that inhibit SARS-CoV-2 replication in vitro and in vivo.
Hohsfield, L.A., K.I. Tsourmas, Y. Ghorbanian, A.R. Syage, S.J. Kim, Y. Cheng, S. Furman, M.A. Inlay, T.E. Lane and K.N. Green (2022). MAC2 is a reliable and long-lasting marker of peripheral-derived myeloid cell CNS infiltrates. Glia, In press.
Olivarria, G.M., Y. Cheng, S. Furman, C. Pachow, M.S. Burns, R.A. Edwards, W. Yong, L. Thompson, L. Hohsfield, C. Smith-Geater, R. Meramontes, C. Manlapaz, J. Teijaro, K.N. Green, and T.E. Lane (2022). Microglia do not restrict SARS-CoV-2 replication following infection of the central nervous system of K18-hACE2 transgenic mice. J. Virology, jvi0196921. doi: 10.1128/jvi.01969-21
Olivarria, G.M. and T.E. Lane (2021). Chemokines and Coronavirus Infection., Expert Rev. Clin. Immunol., 2021 doi 10.1080/1744666X.2022.2017282
Walsh C.M., Plaisted W.C., McIntyre L.L., Loring J.F., Lane TE (2020). Transplantation of iPSC-derived neural progenitor cells promotes clinical recovery and repair in response to murine coronavirus-induced neurologic disease. In iPSCs for Studying Infectious Diseases, Elsevier Press.
Syage, A.R., H.A. Ekiz, D.D. Skinner, C. Stone, R.M. 0'Connell and T.E. Lane. Single-cell RNA sequencing reveals the diversity of the immunological landscape following CNS infection by a murine coronavirus (2020), J. Virology, In press
Mangale, V., A.R. Syage, H.A. Ekiz, D.D. Skinner, Y. Cheng, C.L. Stone, K. Green, R.M. O’Connell and T.E. Lane (2020). Microglia influence host defense and disease following coronavirus infection of the central nervous system. Glia, doi: 10.1002/glia.23844
McIntyre, L.L., S.A. Greilach, O. Shivashankar, I. Sears-Kraxberger, B. Wi, J. Ayala-Angulo, E. Vu, Q. Pham, J. Silva, K. Dang, F. Rezk, O. Steward, M.D. Cahalan, T.E. Lane, and C.M. Walsh (2020). Regulatory T cells promote remyelination in the murine experimental autoimmune encephalomyelitis model of multiple sclerosis following neural stem cell transplant. Neurobiology of Disease, 2020 Apr 7:104868. doi: 10.1016/j.nbd.2020.104868.
Ramstead, A.G., J.A. Wallace, S-H. Lee, K.M. Bauer, W. Tang, J.P. Snook, M.A. Williams, T.E. Lane, J.L. Round, and R. M. O’Connell (2020). Mitochondrial pyruvate carrier 1 (MPC1) enforces T cell homeostasis by enabling pyruvate oxidation in the mitochondria. Cell Reports, 3:30(9):2889-2899.
Skinner, D.D. and T.E. Lane (2020). CXCR2 signaling and remyelination. DNA and Cell Biology, 39(1):3-7
Marro, B.S., D.D. Skinner, J.J. Grist, L.L Dickey, E. Eckman, C. Worne, L. Liu, R.M. Ransohoff and T.E. Lane (2019). Disrupted CXCR2 signaling on oligodendroglia lineage cells enhances myelin repair in a viral model of multiple sclerosis. J. Virology, Jun 26. pii: JVI.00240-19. doi: 10.1128/JVI.00240-19.
Brown, D.G., R. Soto, S. Yandamuri, C. Stone, L. Dickey, J.C. Gomes-Neto, E.D. Pastuzyn, R. Bell, C. Petersen, K. Buhrke, R.S. Fujinami, R.M. O’Connell, W.Z. Shepherd, T.E. Lane*, and J.L. Round* (2019). The gut microbiota protects from viral-induced neurologic damage through microglia-intrinsic TLR signaling (*Co-corresponding authors), eLife, Jul 16;8. pii: e47117. doi: 10.7554/eLife.47117.
Kim, H., L.L. Dickey, C. Stone, J.L. Jafek, T.E. Lane* and D. Tantin* (2019). T cell-selective deletion of Oct1
protects animals from autoimmune neuroinflammation while maintaining neurotrophic pathogen response. J. Neuroinflammation, Jul 3;16(1):133. doi: 10.1186/s12974-019-1523-3.
Grist, J.J., B.S. Marro, C. Worne, D.J. Doty, R.S. Fujinami, and T.E. Lane (2018). Induced central nervous sustem expression of CXCL1 augments neurologic disease in an autoimmune model of multiple sclerosis via enhanced neutrophil recruitment. Eur. J. Immunol. 48(7): 1199-1210, (Cover article).
National Multiple Sclerosis Society CA-1607-25040, Novel approaches towards understanding disease progression and repair using viral models of multiple sclerosis.
NINDS-NIH, R35NS116835, Defining mechanisms of disease and repair in a viral model of multiple sclerosis.
National Multiple Sclerosis Society RG-1907-34532, Stabilizing the blood-central nervous system barrier to treat multiple sclerosis.
R01FD007478 (Xu-PI) Engineered AAV vectors for combinatorial treatment of rare genetic brain diseases This proposal is designed to overcome existing limitations by developing new AAV vectors with effectiveness, quality and safety for CNS-specific gene therapy applications. Role: Multi-PI
Professional Societies
American Association of Immunologists
American Society for Microbiology
American Society for Virology
International Society for Neurochemistry
Other Experience
Graduate Programs
Neurobiology and Behavior

Interdepartmental Neuroscience Program


Cellular and Molecular Biosciences

Immunology and Pathogenesis

Stem Cell Biology

Research Center
Multiple Sclerosis Research Center, Reeve-Irvine Research Center, Institute for Immunology, Center for Virus Research, Stem Cell Research Center
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