Visualizing Tumor Microenvironments: A postdoctoral position is available in the laboratory of Dr. Michael Gerner to investigate how the spatial organization of innate and adaptive immune cells in tumors influences cancer development and the outcome of immunomodulatory therapy. This is an industry-sponsored collaborative opportunity, the major aim of which is to use multiplex confocal imaging and quantitative image analysis (Gerner et al., Immunity 2012, Immunity 2015) to understand tumor microanatomy during disease and after therapy. An additional goal of this project is to develop novel statistical image analysis platforms to better study the spatial relationships and intercellular interactions of cells in complex 3D tissues.

This position requires PhD level training in immunology, cancer biology, or a related field, and/or extensive expertise in imaging and image processing. Experience with bioinformatics and implementation of customized statistical algorithms is desirable. The successful applicant will join a collaborative and dynamic research environment, and will be able to take advantage of the extremely collegial surroundings provided by the UW’s Department of Immunology and the thriving research environment in Seattle. Opportunity has potential for international travel.

Applications should be sent by email to Dr. Gerner at Applicants are requested to send a cover letter, CV, one or two representative publications, and names and contact information of three references.

University of Washington is an affirmative action and equal opportunity employer. All qualified applicants will receive consideration for employment without regard to race, color, religion, sex, sexual orientation, gender identity, national origin, age, protected veteran or disabled status, or genetic information.

Congratulations to Dr. Jeff Duggan for successfully defending his dissertation on Friday, March 10, 2017. His dissertation title is “BCAP functions as a dynamic regulator of hematopoiesis and myeloid cell development."  Dr. Duggan spent his time in the University of Washington Immunology graduate program under the mentorship of Dr. Jessica Hamerman and working in her lab at the Benaroya Research Institute.

Generating protective immunity against the early liver stage of malaria infection is feasible but has been difficult to achieve in regions with high rates of malaria infection. Researchers at the University of Washington (UW) School of Medicine reveal one potential reason for this difficulty in Cell Reports on December 20.Their study demonstrates that exposure to the latter blood stage of malaria infection inhibits the formation of the protective immune cells (and their antibodies) that can prevent the early liver stage infection.

"The blood stage of malaria infection has a very profound impact on the liver stage immune response, and that impact had never been dissected and visualized at this level," says co-author Marion Pepper, UW Medicine researcher and assistant professor of immunology at the UW School of Medicine. "These studies really suggest that you need a vaccine that is protective against both stages of infection to effectively prevent malaria."

To track how the blood stage of malaria infection overpowers the liver stage immune response, Pepper and her collaborators infected two groups of mice with different forms of the malaria parasite. One of these was engineered by their collaborators in the lab of Stefan Kappe, UW affiliate professor of global health and investigator, Center for Infectious Disease Research in Seattle, to stop at the liver stage of infection, while the other progressed to the blood stage of infection. Six days after infection, the researchers found that the levels of antibodies were significantly lower in the mice with the blood stage infection than in mice that only had the parasite targeted to the liver.

To understand this discrepancy, the team tracked the differentiation of Plasmodium liver stage-specific B cells. B cells can differentiate into antibody-secreting early effector cells or long-lived memory cells, both of which contribute to protection against malaria. They discovered that 14 days after infection, the B cells in the blood stage infected mice never went through the necessary changes to make rapidly responsive memory cells. However, in the mice that received the liver-stage attenuated version of the parasite, the B cells were still able to differentiate and create the necessary antibodies and memory cells for an effective immune response.

"This work really highlights the importance of looking at antigen-specific B cells," says Pepper.

"These data also suggest that if you're getting a vaccine while you have an ongoing blood stage infection, there is a chance that the vaccine will not generate good memory cells because the blood stage disrupts all the processes that are involved in making that immunological memory."

Pepper and her collaborators are now looking into the possibility of a drug treatment to solve this problem, as they were able to show that when you treat the second stage of the infection with a drug, the B cells are able to create the optimally responsive memory cells. But for now, the researchers are hopeful that their work can be used to answer immediate questions about the efficacy of malaria vaccines in regions that are most significantly affected by the disease. "Malaria has evolved with us throughout human existence and therefore has some potent immune evasion strategies. We really tried to tease apart some of the factors that could be driving the loss of protective immunity during natural infection and with current vaccine strategies in areas of high malaria transmission," says Pepper. "Our next step is to compare malaria-specific B cells after vaccination or natural infection in humans so we can translate these findings and start to determine how to solve this problem."

This work was supported through the Department of Immunology at the University of Washington School of Medicine and the Center for Infectious Disease Research in Washington.

Read the Cell paper: "Blood stage malaria disrupts humoral immunity to the pre-erthrocytic stage circumsporozite protein."

Article by Cell Press via UW Health Sciences Newsbeat


Congrats to UW Immunology Assistant Professor, Dr. Jakob von Moltke who received the Damon Runyon-Dale F. Frey Award for Breakthrough Scientists. This award provides additional funding to scientists completing the prestigious Damon Runyon Fellowship Award for postdoctoral scholars who have greatly exceeded the Foundation's highest expectations and are most likely to make paradigm-shifting breakthroughs that transform the way we prevent, diagnose and treat cancer. Each awardee will receive $100,000 to be used toward their research.

Successful cancer immunotherapy requires a "type 1" immune response, while "type 2" immune responses have been linked to disease progression and a poor prognosis. As a Damon Runyon fellow, Dr. von Moltke's research has focused on understanding how type 2 immune responses are initiated and regulated, with the hope that insights gained from answering these fundamental questions will lead to improved cancer therapies. He has discovered several novel mechanisms through which type 2 immune responses are initiated, including a critical role for tuft cells—an epithelial cell type that was identified over 50 years ago, but whose physiologic function remained undetermined until now. Dr. Von Moltke's research goals will be to uncover the signals that activate tuft cells, to identify additional effector functions of tuft cells, and to understand how tuft cells work with downstream type 2 effector cells to monitor and regulate tissue homeostasis. 


EVERY COUPLE OF WEEKS, an eagerly awaited package arrives at a University of Washington research lab in South Lake Union. Inside, nestled in dry ice, are special chemical compounds that Dr. Michael Gale Jr. affectionately dubs his “favorite molecules.” These “small molecules” have the potential to stop the Zika virus in its tracks. At the UW’s Center for Innate Immunity & Immune Disease, Gale, ’85, ’94, who is the director, is on the hunt for the right one to constitute a drug to sideline the mosquito-borne illness that has dominated headlines this year, as well as other related viruses. His ace in the hole may be RIG-I, aka retinoic acid-inducible gene I, which was identified in 2005 when he was an assistant professor at the University of Texas Southwestern Medical Center in Dallas. The discovery emerged as Gale and his colleagues were trying to discern how the body triggers an immune response to hepatitis C. RIG-I, they realized, functioned as an “on-off switch” for immunity against the virus. Over a period of years, the researchers figured out that RIG-I kicks into gear when it recognizes and binds to viral RNA, triggering the immune response. Hepatitis C and Zika virus are both RNA viruses (viruses with an RNA genome, as opposed to DNA viruses); so are West Nile, which like the Zika virus infects the brain, and Ebola, which causes deadly hemorrhagic fever—not to mention the common cold and influenza viruses. Gale and the 34 researchers in his lab, in collaboration with Kineta, a local biotech company in which Gale is a founding scientist, are now in the process of testing various small molecules—organic compounds that are tiny enough to infiltrate cells and comprise most drugs—to nail the right formulation to attack these RNA viruses. They’ve screened thousands of molecules to identify a few that activate RIG-I and subsequently induce an immune response that stops the viruses.

Full Article: "Zeroing in on Zika" By Bonnie Rochman 

Read the full article in UW Columns Magazine (page 32).

Congratulations to Dr. Kathleen Pestal for successfully defending her dissertation on Monday, November 21, 2016. Her dissertation title is “The Role of ADAR1 in Innate Immune Regulation and Cell Biology.”  Dr. Pestal spent her time in the University of Washington Immunology graduate program under the mentorship of Dr. Dan Stetson and working in his lab at UW Medicine's South Lake Union Campus.

Congratulations to Dr. Mike Stolley for successfully defending his dissertation on Thursday, November 17, 2016.  His dissertation title is “33D1+ DCs in Tolerance and Immunity.” Dr. Stolley spent his time in the University of Washington Immunology graduate program under the mentorship of Dr. Dan Campbell and working in his lab at the Benaroya Research Institute and UW Medicine South Lake Union Campus.

Congratulations to Dr. Akshay Krishnamurty for successfully defending his dissertation on Wednesday, November 2, 2016.  His dissertation title is “Development and function of Plasmodium-specific memory B cells during blood stage malaria infection.” Dr. Krishnamurty spent his time in the University of Washington Immunology graduate program under the mentorship of Dr. Marion Pepper and working in her lab at UW Medicine's South Lake Union Campus.

It has been an excellent year for the Immunology Department and we want to share some of our news with you in our annual newsletter. We also want to thank our students, postdocs and research scientists for their talents, hard work and energy that has allowed our research to flourish, and for making this a fun place to work and learn.Thanks also to our administrative staff for supporting everything we do, and handling the challenges of running a complex enterprise with a high degree of professionalism.

Finally, we greatly appreciate those who have donated to us this past year in support of our efforts; we have put your resources to good use. To donate this year there is a link within the newsletter or click here, your support is critical to us in helping us achieve our mission.

Courtesy of the Center for the Study of Hepatitis C, The Rockefeller University Electron micrograph of hepatitis C virus purified from cell culture. Scale bar is 50 nanometers. The virus that causes hepatitis C protects itself by blocking signals that drive elements of liver cells’ immune defenses, University of Washington researchers report in a new study.

“The finding helps explain why many patients fail certain drug treatments, and should help develop more effective alternate treatment protocols,” said Ram Savan, the study's corresponding author and an assistant professor of immunology in the UW School of Medicine.

Hepatitis C virus is the most common cause of chronic hepatitis and the leading U.S. cause of liver cancer. It is primarily spread through contact with infected blood. Each year, more than 30,000 Americans become infected and as many as 85 percent develop life-long chronic infections. Of these patients, about one in 10 will eventually develop cirrhosis and liver cancer.

In the new study, lead author Abigail Jarret, now a grad student at Yale University, and colleagues showed that hepatitis C virus sabotages liver cell antiviral defenses by blunting the effect of key immune proteins called interferons. When cells become infected, they release interferons, which in turn spur hundreds of genes that generate virus-fighting proteins within the cell. Interferons can even cause cells to self-destruct to prevent the virus from propagating.

One of these interferons, called interferon-alpha, has been used for many years to treat chronic hep C virus infections, either alone or in concert with an antiviral called ribavirin. These treatments helped many patients clear their virus, but the treatment fails to cure more than 60 percent of patients.

Newer, more effective drugs with fewer side effects have now largely replaced interferon-based therapies. However it was not clear why interferon treatment failed so often. In their study, the UW researchers hypothesized that the virus' ability to evade interferons was related to the cells themselves.

In a previous study (, Savan’s research team discovered that when hepatitis C virus invades a liver cell, the virus induces the cell to activate two genes -- MYH7 and MYH7B -- that are usually active only in smooth skeletal muscle and cardiac cells. Once activated, these genes produced two microRNAs, molecules that can interfere with the production of other proteins. Savan and colleagues showed that these microRNAs interfered with the cell’s production of two interferons. Thus, by activating the MYH7 and MYH7B genes, the invading hep C viruses limit liver cells' ability to generate these interferons and blunt the cells’ ability to resist and clear the virus.

In the new study, published today in Nature Medicine, the investigators showed that these virally- induced microRNAs also inhibit production of a receptor crucial to the cell's interferon-driven antiviral response.

 See the UW Health Sciences Newsbeat Article.

  Article By Michael McCarthy | HSNewsBeat | Updated 12:00 PM, 11.14.2016 Posted in: Research ( 

Ram Savan is a UW assistant professor of immunology in the UW School of Medicine.