"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.
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.
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
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.
4th Aegean conference on the crossroads between innate and adaptive immunity.
Nat Immunol. 2011
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. 2011
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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