Elina Zuniga

Research

The immune system is responsible for the tremendous task of fighting a wide range of pathogens to which we are constantly exposed. This system can be broadly subdivided into innate and adaptive arms, which act in conjunction to protect the host. The innate immune system exists in both vertebrate and invertebrate organisms and represents the first barrier against microbial invasion. This arm of the immune system rapidly eliminates the vast majority of microorganisms that we daily encounter and is responsible for limiting early pathogen replication and imprinting the profile of the subsequent adaptive response. The adaptive immune response is a more sophisticated feature, found only in vertebrate animals, involving a broad repertoire of genetically rearranged receptors that specifically recognize microbial antigens. The hallmark of the adaptive response is the generation of a potent and long-lasting protection specifically directed against the invading pathogen. Despite highly evolved immune responses, pathogens have co-evolved ways to evade or subvert the immune system to favor their replication and transmission. Therefore, despite major scientific and medical efforts, infectious diseases remain among the leading causes of mortality and disability worldwide. Dramatic examples of microbial immune-evasion are chronic viral infections such as Human Immunodeficiency virus, Hepatitis B and C viruses, which currently infect about 500 million people around the world.

Our laboratory studies cellular and molecular aspects of immune responses during acute and chronic viral infections to determine general principles of antiviral immunity, immune-evasion, persistence and pathogenesis. We use a combination of both standard and cutting-edge molecular approaches as well as functional assays with recombinant viruses and genetically modified hosts. Both hypothesis driven and unbiased strategies allow us to unravel novel aspects of host-virus interactions in mouse models of natural viral infections that we aim at translating to humans. The ultimate goal is to generate fundamental knowledge on immune-regulation that could help modulating immune responses to prevent or treat infectious diseases and may have implications for other immune-related illnesses.

Publications

Full list on PubMed
  • G. Lewis, E. Wehrens, L. Labarta-Bajo, H. Streek and E. Zúñiga. TGFß Receptor Suppresses Eomesodermin and Maintains CD4 T cell Identity during Chronic Viral Infections. Journal Of Clinical Investigation. 2016. 126(10):3799-3813.
  • M Macal, MA Tam, C Hesser, J Di Domizio, P Leger, M Gilliet and E Zuniga. CD28 Deficiency Enhances Type I IFN Production by Murine Plasmacytoid Dendritic Cells. Journal of Immunology. 2016. 196(4):1900-9.
  • A. Taylor, J. Harker, P. Stevenson, E. Zuniga and C. Rudd. Glycogen synthase kinase 3 (GSK-3α/β) is the central upstream kinase responsible for PD-1 transcription in T-cells. Immunity. 2016. 44(2):274-86.
  • G. Lewis, E Wehrens, L Labarta-Bajo, Hendrik Streek and E. Zuniga. TGFß Receptor Suppresses Eomesodermin and Maintains CD4 T cell Identity during Chronic Viral Infections. Journal Of Clinical Investigation. 2016. 126 (10):3799-3813.
  • E. Zúñiga, M. Macal, G. Lewis and J Harker. Innate and Adaptive Immune-regulation During Chronic Viral Infections. Annual Reviews Of Virology. September 2015.
  • J. Harker*, K. Wong*, A. Dolgoter and E. Zúñiga. Cell-Intrinsic gp130 Signaling on CD4+ T Cells Shapes Long-Lasting Antiviral Immunity. Journal of Immunology. 2015. 195(3):1071.
  • J. Harker, A. Dolgoter, E. Zúñiga. Cell-intrinsic IL-27R/gp130 signaling regulates virus specific CD4 T cell responses and viral control during chronic infection. Immunity. 2013. 39(3): 548
  • M Macal, G.M. Lewis, S Kunz, RA. Flavell, J. Harker and E. Zúñiga. Plasmacytoid Dendritic Cells Are Productively Infected and Activated through TLR-7 Early After Arenavirus Infection. Cell Host & Microbe. 2012. 11(6):617-30. (Commented in Cell Host & Microbe, 2012, 11(6):553-5.).
  • J. Harker, G.M. Lewis, L. Mack, E. Zúñiga. Late Interlukin-6/ escalates T follicular helper cell responses and controls chronic viral infection. Science. 2011. 11;334(6057):825-9. (Editor Choice. Sci. Signal. 4, ec321-2011).
  • R Tinoco, V Alcalde, Y Yang, K Sauer and E Zúñiga. Cell-Intrinsic Transforming Growth Factor- Signaling Mediates Virus-Specific CD8+ T Cell Deletion and Viral Persistence In Vivo. Immunity. 2009. 31(1): 145-157. (Commented in Science-Business eXchange (SciBX) 2009, 2 (29):14).
  • E Zúñiga, L Liou, L Mack, M Mendoza and MBA Oldstone. Persistent virus infection inhibits type I interferon production by plasmacytoid dendritic cells to facilitate opportunistic infections. Cell Host & Microbe. 2008. 16 (4):374-86. (Commented in Cell Host & Microbe, 2008, 4 (16):305 and Nature Reviews Immunology, Research Highlight 2008, 8:908).
  • E Zúñiga*, H Lauterbach*, P Truong, MBA Oldstone, and DB McGavern. Adoptive immunotherapy induces CNS dendritic cell recruitment and antigen presentation during clearance of a persistent viral infection. Journal of Experimental Medicine. 2006. 7;203(8):1963. (*denotes equal contribution).
  • E Zúñiga, DB McGavern, JL Pruneda-Paz, C Teng, and MBA Oldstone. Bone marrow plasmacytoid dendritic cells can differentiate into myeloid dendritic cells upon virus infection. Nature Immunology. (Selected for cover and commented in Nature Immunology, 2004, 5 (12):1206). 5:1227-1234, 2004.

Biography

Elina Zuniga received her Ph.D. in Biochemistry from the National University of Cordoba, Argentina. She conducted postdoctoral research at The Scripps Research Institute where she held two post-doctoral fellowships from Antorchas Foundation and PEW Charitable Trust, respectively. After joining UCSD in 2007 she has received a Hellman Foundation Scholar Award, The Vilcek Finalist Prize for Creative Promise, the Leukemia and Lymphoma Society Scholar Award and the American Cancer Society Scholar Award (a lifetime honor).