The Goga Lab’s research focuses on three main immunological goals: First, their lab studies basic aspect of cancer biology, including how do specific oncogenes alter tumor-immune interactions. For example, they have discovered that MYC-driven breast cancers may regulate the tumor microenvironment via cell intrinsic and extrinsic effects. They are currently exploring how extracellular vesicle (EV) contents of MYC-driven breast tumors effect the composition of tumor immune composition. Secondly, their group explores patient response to combined targeted and immune therapies as participants in several clinical trials. Third, they explore in cancer and immune metabolic alterations, which may be new anti-cancer therapeutic approaches.

The Goldberg lab studies how crosstalk between the immune and metabolic systems coordinates immune function, inflammation, and chronic disease. Specifically, they propose a bi-directional circuit in which (a) immune cell activation and inflammatory potential is dictated by the metabolic environment, and (b) immune cells modify metabolic organ function to impact systemic metabolic health.

The Graham lab's field of research is the study of how host immunity drives pulmonary vascular disease, focusing on the disease schistosomiasis-associated pulmonary hypertension (PH). Schistosomiasis is a major cause of PH worldwide, but how this parasitic infection causes the disease is unclear. We think that some of the pathways that we are uncovering are relevant to other forms of PH more common in developed settings. Our primary approach is using a mouse model of this disease, which lends itself well to investigating how innate and adaptive immunity, and the cross-talk between the two, mechanistically drive pulmonary vascular disease. The pathway we have uncovered includes conventional dendritic cells, CD4 T cells, classical monocytes, and interstitial pulmonary macrophages, expressing cytokines including IL-4/IL-13, CCL2, TSP-1, and TGF-beta. We are now starting to develop protocols for screening humans for this disease in endemic settings, and studying biospecimens from these individuals. We are also studying the role of inflammation in hypoxic-PH and other forms of PH.

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.