Jason Cyster
Antibody responses are important for protection from extracellular pathogens. The Cyster lab studies the induction of Germinal Center and plasma cell responses to various antigens as well as the mechanisms guiding the trafficking of effector lymphocytes.

Other Research in Dr. Cyster's Lab
Diabetes and Autoimmunity • Development and Differentiation • Immune Regulation • Immune Receptors and Signaling

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Joanne Engel
The Engel lab is interested in the interactions between microbial pathogens and host cells. We use genetic, cell biologic, genomic, and immunologic techniques to study two important bacterial pathogens, Pseudomonas aeruginosa and Chlamydia trachomatis.

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Nigel Killeen
We are studying the immune response to a chronic airway infection (Mycoplasma pulmonis) with a view to understanding the basis of vascular remodeling in the context of a persistent adaptive immune response. We also routinely use other microbial and viral systems to inform on how immune responses might be dependent on specific signaling and regulatory processes. Part of this work involves determining how specific kinds of signals elicited during pathogen-specific immune responses favor the formation of long-lived protective memory cells, and thus are beneficial in the context of vaccination.

Other Research in Dr. Killeen's lab:
Allergy and Asthma, Diabetes and Autoimmunity, Development and Differentiation, HIV and Viral Immunity, Immune Regulation, Immune Receptors and Signaling

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Richard Locksley
We use a variety of microbial pathogens, including Leishmania, Listeria and Nippostrongylus, to model the acquisition of stable cytokine phenotypes by helper T cells in vivo. Our interests involve unraveling mechanisms that position cells in critical areas together and the orchestration of their effector function.

Other Research in Dr. Locksley's lab:
Development and Differentiation • Imune Regulation • Inflammation

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Averil Ma
Our work on intracellular mechanisms of coordinating signal transduction events has focused on the molecule A20. Tumor necrosis factor (TNF) is a pleiotropic pro-inflammatory cytokine that stimulates multiple cellular activation and survival signaling pathways. By targeting the TNF induced A20 gene, we found that A20 deficient mice develop profound autoimmunity coupled with an inability of A20 deficient cells to terminate TNF induced NF-kB responses (Lee et al, Science 2000). We subsequently generated A20 TNF and A20 TNFR double mutant mice, and found that A20 is critical for regulating toll-like receptor (TLR) induced NFkB signals that commit both innate and adaptive immune responses (Boone et al, Nature Immunology 2004). Moreover, we have found that A20 is also critical for terminating JNK signals. Thus, A20 mediates cross-talk between NFkB and JNK signaling pathways. Moreover, we have found that A20 is a unique ubiquitin modifying enzyme that requlates both the activity and stability of signaling proteins Wertz et al, Nature 2004; Boone et al, Nature Immunology 2004). A20 is thus a biochemically unique molecule that is critical fro regulating multiple signaling pathways and biological processes that depend on these pathways. Recent studies indicate A20 is expressed in T cells and dendritic cells, and may play critical roles in regulating both innate and adaptive immune responses. Ongoing studies focus on the physiological targets of A20’s enzymatic activity, the biochemical mechanisms by which A20 functions, the regulation of A20 activity, and the roles of A20 in regulating T cell and dendritic cell activation and survival. Experiments related to microbiology will examine the role of A20 in regulating macrophage and dendritic cell response to model infectious organisms (e.g., Listeria).

Other Research in Dr. Ma's Lab
Immune Regulation • Immune Receptors and Signaling • Inflammation • Diabetes and Autoimmunity

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James McKerrow
My laboratory is interested in the interaction between eukaryotic parasites and the host immune system. We are focusing on two classes of organisms. The first are intracellular parasites exemplified by Leishmania and Trypanosoma cruzi. We are defining how they evade the host immune response during their residence in host macrophages. Our second area of interest is how the complex schistosome blood fluke alters its developmental program depending upon the status of the host immune response.

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William Seaman
We demonstrated that TREM-2, a receptor that is induced during macrophage activation, binds broadly to bacteria and to some fungi. We are therefore studying the role of this recognition in host defense against pathogens.

Other Research in Dr. Seaman's lab:
Immune Receptors and Signaling • Tumor Immunology • Autoimmunity

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Anita Sil
H. capsulatum survives and replicates in the phagosome or phagolysosome of macrophages. How this fungus colonizes an intracellular niche that is normally hostile to microbes is a mystery. The ability of H. capsulatum to prevent acidification and maturation of the phagosome is thought to play an important role in survival in macrophages. We hypothesize that H. capsulatum produces gene products that block phagosome maturation and acidification. One of our main research goals is to use molecular genetic approaches to uncover which pathogen molecules are required to inhibit phagosome maturation. We are also using functional genomics to decipher which host genes are manipulated by the pathogen. We are part of a program project grant to study the immune response to intracellular pathogens, so this work is informed and influenced by studies of the interaction of host cells with Listeria monocytogenes, Mycobacterium tuberculosis, and Francisella tularensis in the in the laboratories of Dan Portnoy (UC Berkeley), Jeff Cox (UCSF), and Denise Monack (Stanford), respectively. A comparative analysis of approaches employed by these four intracellular pathogens will allow us to contrast strategies employed by a diversity of microbes.

Other Research in Dr. Sil's lab:
Immune Receptors and Signaling

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Zena Werb
We are using intravital confocal microscopy in to investigate the mechanisms underlying the extravasation, chemotaxis and responses of leukocytes to microorganisms in normal and mutant mice.

Other Research in Dr. Werb's lab
Inflammation • Tumor Immunology • Development and Differentiation

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