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“From a clearer understanding of how T cell memory works will come new therapies for cancer, autoimmunity, and viral diseases. ”
Stephen Schoenberger, Ph.D.
Division of Developmental Immunology

cell-bullet1.jpg"Mainstream cancer treatments such as chemotherapy, radiation and surgery remain important, but there is also strong interest in finding ways to educate the immune system to attack and destroy cancerous cells." - Stephen Schoenberger, Ph.D.

Stephen Schoenberger, Ph.D.Dr. Schoenberger joined LIAI in 1998 as an Assistant Professor in the Division of Immune Regulation. In 2002, Dr. Schoenberger became an Associate Professor in the Division of Cellular Immunology, and in 2005 gained Tenure. In 2008, he was promoted to Professor. Dr. Schoenberger's research focuses on the regulation of cellular immune responses.

Dr. Schoenberger received his B.S. from the University of California, Los Angeles in 1987 and his Ph.D. from the same university in 1992. In 1993, Dr. Schoenberger was a Postdoctoral Fellow in Immunohematology at the University of Leiden Hospital, the Netherlands, from 1993-1998.

Dr. Schoenberger is a member of numerous grant review panels and a reviewer for many scientific publications. He is also a member of the editorial advisory board for the Journal of Experimental Medicine.

research focus

cell-bullet2.jpg When the immune system detects the presence of a dangerous invader such as a pathogenic virus or bacterium, it often takes the drastic action of killing any cell bearing signs of having been infected. For certain threats, this task is assigned to a subset of "killer" (cytotoxic) T lymphocytes (CTL). When exposed to a specific antigen, CTL undergo a rapid series of divisions and migrate to the site of infection to begin destroying infected cells. Once the threat has been eradicated, the majority of the CTL will undergo programmed death, except for a small fraction, perhaps 5 to 10 percent that will persist for years as "memory" CTL able to mount a rapid secondary response should the same pathogen be encountered. Properly controlled, CTL can confer protective immunity to a wide variety of infectious organisms and can even be instructed to attack tumors or latent viruses that attempt to hide from the immune system. Loss of CTL regulation, however, can result in unwanted destruction of healthy tissue and pathogenic autoimmunity. The laboratory is trying to understand the rules by which CTL are activated and regulated, and the degree to which they can be harnessed for therapeutic goals.

The labs efforts are currently divided into three main areas. One of these concerns the role of CD4+ 'helper' T lymphocytes in regulating CTL responses. The second area of investigation concerns the elucidation of the instructional program that guides CTL development and the signals through which it can be modified. The third area of investigation involves the mechanisms through which the immune system remains tolerant to self-tissues while retaining the capacity to mount a vigorous response against a dangerous virus or bacterium. The long-term goal is to acquire a mechanistic understanding of the signals guiding CTL activation, development, and memory such that they can be strategically manipulated in to combat human diseases such as cancer, diabetes, MS, and AIDS.

selected publications


4th Aegean conference on the crossroads between innate and adaptive immunity.
Nat Immunol.

Immune adjuvant efficacy of CpG oligonucleotide in cancer treatment is founded specifically upon TLR9 function in plasmacytoid dendritic cells. Cancer Res. 2011

Mucosal memory CD8(+) T cells are selected in the periphery by an MHC class I molecure.
Nat Immunol. 2011

Interleukin-2 rescues helpless effector CD8(+) T cells by diminishing the susceptibility to TRAIL mediated death. Immunol Lett. 2011

Autocine IL-2 is required for secondary population expansion of CD8(+) memory T cells.
Nat Immunol.

Sustained antibody responses depend on DC28 function in bone marrow-resistent plasma cells. J Exp Med. 2011

B cell-specific expression of b7-2 is required for follicular th cell function in response to vaccinia virus. J Immunol. 2011

Differential B7-CD28 costimulatory requirements for stable and inflationary mouse cytomegalovirus-specific memory CD8 T cell populations. J Immunol. 2011

From the loading dock to the boardroom: a new job for Akt kinase. Immunity. 2011

The TNFR family members OX40 and CD27 link viral virulence to protective T cell vaccines in mice. J Clin Invest. 2011

B7-mediated costimulation of CD4 T cells constrains cytomegalovirus persistence.
J Virol. 2011

TRAIL-expressing CD8+ T cells mediate tolerance following soluble peptide-induced peripheral T cell deletion. J Leukocyte Biol. 2010

Enhancement of proliferation and downregulation of TRAIL expression on CD8+ T cells by IL-21. Eur J Immunol. 2010 

Distinct roles of cytolytic effector molecules for antigen-restricted killing by CTL in vivo. Immunol Cell Biol. 2010

Separate roles for antigen recognition and lymph node inflammation in CD8+ memory T cell formation. J Immunol. 2010

The 2010 Midwinter Conference of Immunologists at Asilomar. Nat Immunol. 2010

Plasticity in programming of effector and memory CD8 T-cell formation. Immunol Rev. 2010

Effectors and memories: Bcl-6 and Blimp-1 in t and B lyphocyte differentiation.
Nat Immunol. 2010

Memory T Cells. Adv Exp Med Biol. 2010

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upcoming seminars
    "Zinc-induced Polymerization of Receptor at the Plasma Membrane: A New Form of Regulated Signal Transduction?"
    Wednesday 05/18/16: 12:00 PM
    "Exploring the Roles of Type-2 Cytokine-producing Mucosal Mast Cells in Allergic Disorder"
    Wednesday 06/01/16: 12:00 PM
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