The Laszik Lab uses novel tissue-based methods to study inflammation, in situ. We have developed and optimized a number of highly reproducible and quantitative morphologic assays on transplant kidney biopsies that utilize novel technologies such as whole slide digital imaging computer assisted image analysis, multiplexing immunofluorescence microscopy, and new generation in situ hybridization. This approach is a conceptual innovation to assess the pathologic changes in various tissues, including cancer, with advantages of combined immunophenotypical and gene expression analysis without losing the benefits of the histologic-structural context. In addition, we are actively working on bulk gene expression profiling in correlation with detailed morphologic analysis and are developing cell dissociation technologies on the kidney to pursue single cell RNAseq.

Dr. Chan is a Project Manager and Senior Scientist for Immunoprofiler.Among other projects, Immunoprofiler uses tumor biopsies taken from patients to intensively analyze their immune composition and divide the immune response into subclasses that define the disease. We aim to make maximal use of donated tumor tissue, immediately bring it to the laboratory upon its removal. By taking it live and intact, we have the opportunity to study it much more intensely. Tumor cells and immune cells continue to interact in these sections for many hours and they use technology developed at UCSF to study this using multiple kinds of tests, such as quantifying immune cells at the edge or center of the tumor and subjecting them to live tumor imaging in order to view how the cells behave.

The Piao Lab investigates the molecular mechanisms underlying those diverse functions of microglia with a special focus on how they refine the brain circuit by regulating interneuron development and synaptic pruning. Microglia act as resident brain cells in regard to their involvement with neurogenesis, synapse refinement and modulation of neural circuits. At the same time, microglia express their macrophage ontogeny by virtue of responding to Damage Associated Molecular Patterns (DAMPs) generated by disease processes, aging and cell injury. The canonical macrophage-like responses of microglia may be reparative, injurious or maladaptive during neurodevelopment or neurodegeneration. Relatively little is known in molecular detail about these aspects of microglial physiology particularly in humans, yet the genetic architecture of neurodegenerative disease illustrates vividly that microglial responses can be crucial for the divergent trajectories of healthy development or aging versus disease.�

The Fidler Lab studies of CH have underscored the importance of dysfunctional Mfs to atherosclerosis pathogenesis; therefore, our second focus aims to identify novel factors which promote the accumulation of Mfs in plaques. These studies expand on the labs findings in mice modeling JAK2 CH where we found that the percent of Mfs harboring Jak2 mutations in lesions doubled relative to the burden of mutated monocytes in blood, indicating that either monocytes/Mfs with mutations enter the lesions at a higher rate, proliferate more, or survive longer than WT cells in the same mouse1.�

The DeFranco lab studies receptor signaling in immune cells with a focus on the B cell antigen receptor (BCR) and Toll-like receptors (TLRs). In a longstanding collaboration with Clifford Lowell (UCSF), we have also studied the role of the Src-family kinase Lyn in inhibitory receptor signaling in B cells and the autoimmune disease that develops in Lyn-deficient mice. To study the in vivo function of TLRs in mice, we made a conditional (Cre/loxP) allele of the TLR signaling component MyD88 and have used this tool to characterize the role of MyD88 in dendritic cells and B cells for innate and adaptive immune responses. In recent years, we have discovered that BCR and TLR signaling reactions synergize to promote the germinal center response.

The Deuse Lab aims to define and understand the different facets of this immune barrier as such we were the first to describe the antigenicity of mitochondria in somatic cell nucleus transfer (SCNT)-derived embryonic stem cells. We have further presented our concept of engineered, hypoantigenic PSCs as a strategy to circumvent immune rejection of incompatible cell grafts. Pluripotent stem cells (PSCs), which include both embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs), are defined by their self-renewal and pluripotent potential, which makes them excellent candidates for regenerative therapies. However, despite their seemingly unlimited ability for growth and differentiation, immunological problems are among the hurdles currently preventing broader use of PSCs for translational therapeutic purposes.

The Scharschmidt Lab studies the cellular and molecular mechanisms mediating the adaptive immune response to skin commensal bacteria in order to elucidate the role of microbes in skin homeostasis and inflammatory skin disease. Research in our lab aims to: 1) define host pathways and immune cell populations that facilitate establishment of adaptive immune tolerance to skin commensals; 2) identify commensal-derived molecules that influence the development and function of adaptive immune cell populations in the skin; 3) elucidate how skin-specific structures, such as hair follicles, and the integrity of the skin barrier influence host-commensal dialogue in this tissue. Our scientific approach capitalizes on genetic manipulation of skin commensal bacteria, transcriptional profiling of both host and microbial cells and in vivo models to dissect the antigen-specific response to skin commensal organisms.

The������MacKenzie������Lab is focused on understanding maternal-fetal immunology with the goal of treating patients with birth defects using in utero stem cell transplantation. We also study the immune basis of pregnancy complications that arise due to a breakdown in maternal-fetal tolerance, such as preterm labor. We work on mouse models as well as patient samples and have a robust program

The Tlsty Lab���������s main focus is on chronic inflammation, and its connection to cancer. Globally, an astounding 20-25% of cancers are linked to chronic inflammation, including cancers of the esophagus, bowel and pancreas. We are determining whether it's possible to treat the inflamed cells and tissues surrounding a tumor, rather than directing therapies at the tumor itself. Our project aims to find novel ways of treating cancer that has been caused by inflammation, and develop new options to prevent cancer developing in high-risk patients with chroni

The central goal of Dr. Arnold's research is to investigate overlapping mechanisms of brain development and disease. His lab is especially interested in understanding how microglia, the primary immune system cell of the brain, are developmentally programmed, and how these cells may mitigate or produce brain injury. Dr. Arnols has discovered that abnormal microglia programming in mice leads to anatomic and phenotypic features of cerebral palsy, the most common movement disorder in children. Using cutting-edge molecular/genetic tools, he and his team are dissecting core microglia activation gene networks, with the goal of identifying new treatment targets for this devastating disease. His work is directly relevant to ImmunoX neurodegeneration and potential pilot CoProjects.

The Peng Lab is interested in how supportive niche cells modify the regenerative capacity of the stem cell, with the goal of deciphering cellular crosstalk that drives adaptive tissue regeneration. Our lab utilizes the lung as a model organ due to its immense cellular diversity and architectural complexity. Adult solid organs are composed of diverse cellular compartments with complex 3D organization that informs specific functions, with varying degrees of regenerative capacity in response to injury and tissue inflammation. While resident tissue stem cells play an important role in the regenerative process, they are located within a cellular ecosystem composed of various cell types that regulate stem cell function, including immune cells.

The Lynch Lab���������s research focuses on the role of the microbiome in promoting immune dysfunction and chronic inflammatory diseases of the gastrointestinal and respiratory tracts. The human superorganism represents a coalition of man and microbes, with the greatest diversity and burden of these species concentrated in the lower gastrointestinal (GI) tract. Leveraging human population-based observations to inform in vitro and in vivo experimental models, we dissect microbial-host interplay in the context of inflammatory sequelae. Research in the Lynch laboratory addresses key areas of human microbiome research: 1) Early-life microbiome functional development, immune training and childhood asthma 2) Gut-airway axis 3) Molecular mechanisms of microbial-medi

The Lee Lab performs HIV translational genetics and immunology research in a multi-disciplinary�"bench-to-bedside"��research program. This includes large-scale host genetic epidemiologic studies as well as clinical trials research focused on pharmacogenomics and precision medicine. Methods applied in our research includes performing genomewide, whole exome sequencing, single cell sequencing (transcriptomic and immunophenotypic expression), as well as host-pathogen (HIV integration site) analyses. The primary goals of our research is to integrate advanced genetic and immunologic technologies to identify potential novel targets for the prevention and treatment of infectious diseases, such as HIV and SARS-CoV-2 infection.