The Greenland Lab is focused on the immunology and cell biology mechanisms that underlie chronic lung allograft dysfunction (CLAD), the primary limitation to long term survival following lung transplantation. Their group has defined novel roles for effector and regulatory T cells, NK cells, and macrophages in the allograft at the time of rejection. The lab has published on the role of immune aging and telomere dysfunction in shaping the alloimmune response. Their work leverages genomics and bulk, single cell, and spatial transcriptomics, in collaboration with the ImmunoX CoLabs, UCSF Departments of Medicine and Surgery, and collaborators across the globe. As a disease-focused, translational immunology lab based at UCSF Parnassus campus and the San Francisco VA, they are theyll positioned to contribute to ImmunoX.

The He Lab is dedicated to developing computational methods and profiling transcriptomic and chromatin changes with spatial contexts. They aim to construct ultra-high resolution cell atlases of healthy and altered tissues and organoids, to dissect the intricate relationships bettheyen genes, cells and tissues. The computational frameworks they are building are theyll-suited to address key challenges faced by the ImmunoX community.

The Hellman Lab is focused on basic and translational research on sepsis and other forms of inflammation-driven acute organ failure ("Inflammatory Critical Illness"). Sepsis and multiple organ failure are leading causes of death in the Intensive Care Unit. These processes result from a complex inflammatory response that is initiated through the innate immune system by interactions bettheyen host cells and microbes or endogenous host factors that are released during injury or cell death. The family of Toll-like receptors (TLRs) recognize different microbial components and endogenous host factors, and are critical in initiating inflammatory responses to infection. They study TLR-dependent pathways expressed by macrophages as theyll as non-conventional inflammatory cells, including endothelial cells, in Inflammatory Critical Illness, focusing on their roles in coagulopathy, vascular permeability, neutrophil trafficking to organs, and organ injury and failure.

The Hermiston Lab is focused on defining the underlying mechanisms in the development of lymphoid malignancies, including leukemia and lymphoma.

The Hollenbach lab specializes in genetic analysis of the extremely polymorphic human leukocyte antigen (HLA) and killer immunoglobulin-like receptor (KIR) immunogenetic systems. Their work spans the population genetics, evolutionary history, and influence on human health of these complex genomic regions, with particular emphasis on their role in neurological disease.

The Hunt Lab focuses on the causes and consequences of persistent immune activation during treated HIV infection, including its contribution to age-related morbidity and HIV persistence. The lab also has a particular focus on the contribution of asymptomatic CMV co-infection to the inflammatory state and morbidity in this setting, leveraging samples from and contributing to the design of clinical trials on this topic.

The Javid Lab's research includes study of protective human humoral responses to tuberculosis, as well as molecular mechanisms by which Mycobacterium tuberculosis adapts and evades host immunity. We use animal models, forward genetics and cell biology to investigate the mechanisms by which antibodies may contribute to protection of tuberculosis and the rational design of novel preventative and therapeutic TB vaccines. Our work challenges the decades-old paradigm regarding the relevance of antibody-mediated immunity to tuberculosis. Furthermore, we have identified pathogen-derived mechanisms by which M. tuberculosis adapts to the host environment, including dysregulation of innate and adaptive immunity. Our work combines both hypothesis-driven and agnostic, hypothesis-generating approaches to better understand both the fundamental host-pathogen interaction in tuberculosis as well as identify translationally relevant approaches for novel treatments and vaccines.

The Kamber Lab is interested in understanding how macrophages detect and eliminate unwanted cells in cancer and other aging-related diseases. Current efforts in the lab focus on 1) systematically identifying the inter-cellular signaling pathways that enable macrophages to recognize and destroy target cells and 2) engineering macrophages with enhanced capabilities for therapeutic cell clearance. To advance these studies, they combine potheyrful genetic screening approaches to discover molecules that regulate macrophage function with biochemical, cell biological, and in vivo experiments to understand how these components work at a mechanistic level. Their overarching goal is to uncover new biological insights that enable next-generation immunotherapies for currently untreatable diseases.

The Kattah Lab studies how various genes and diverse cell types lead to Inflammatory Bowel Disease (IBD). We have a particular interest in the role of intestinal epithelial cells in IBD. We are using a variety of techniques including multiplex single-cell RNA sequencing, flow cytometry, and culture of intestinal organoids to study patient samples and mouse models of disease.

Dr. Keenan is a physician scientist who works in translational cancer research and medical oncology. Her research interests are in studying the mechanisms of response and resistance to immunotherapy, with a focus on gastrointestinal cancers. Her clinical practice is in the Cancer Immunotherapy Clinic, where she leads early phase immunotherapy trials of novel agents including cell therapies, vaccines, checkpoint inhibitors, and T cell engagers.

The Kotas Lab is interested in the mechanisms by which structural cells such as epithelial cells and immune cells communicate to enable effective barrier defense and promote proper functioning of the airway. The lab is focused on type 2 inflammation, but their overarching interest is in common inflammatory mediators and converging pathways that facilitate homeostasis or produce airway inflammation during various environmental challenges. For example: Can they define shared inflammatory signals that induce airway mucus overproduction in COPD and asthma? What immune cues can promote barrier integrity in response to both bacteria and allergens? How do tissue parenchymal cells remember and adapt to prior insult? Anstheyring these questions could enable their understanding of fundamental principles of airway biology and facilitate development of therapies to target common pathological mediators in common airway inflammatory diseases.

The Krummel Lab focusses on understanding patterns of immune cell-cell interactions and how these generate “the immune system”. Their studies of the immune synapse have shown how T cells regulate their motility, how they signal through synapses while moving, how they communicate with each other during arrest, and how they ‘search’ a new tissue. These are all fundamental findings and provide a lens through which they understand T cell function. Over the past ftheir years, they have developed novel methods and computational platforms to understand immunological processes in space and in time within normal and diseased organs. They theyre the first to live-image events in progressive tumors in which incoming tumor-specific T cells are captured by a population of myeloid cells. Dr. Krummel is tremendously excited that they have begun to develop a pipeline of next-generation protein immuno-therapeutics using imaging to ‘guide’ this development. Concurrently, they co-developed a imaging technologies that allow, for the first time, observation of the immune system in the homeostatic, infected/injured, allergic or metastatic lung. As with primary tumors, this latter focus has allowed them to dismiss many hypothetical immune scenarios and intensely study those that define the biology in situ. These studies define how the immune system is organizing over space and time and guides novel therapeutic solutions.