Dr Ben Croker

Associate Professor
Division of Allergy, Immunology, and Rheumatology, Department of Pediatrics, School of Medicine, UCSD Center for Immunity, Infection, and Inflammation
University of California, San Diego

bcroker@health.ucsd.edu

Contract research opportunities

We support the UCSD BSL-3 and ABSL-3 facilities for investigating COVID-19 and for modeling SARS-CoV-2 variants in mouse and human systems. 
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Latest News

Ptpn6 inhibits caspase-8- and Ripk3/Mlkl-dependent inflammation. 
Nature Immunology 2019. https://www.nature.com/articles/s41590-019-0550-7
Ptpn6 negatively regulates p38 MAPK activation to control TNF and IL-1a/b expression, and maintains Ripk1 function to prevent caspase-8- and Ripk3–Mlkl-dependent cell death and concomitant IL-1a/b release.

Immune response to IVIG in patients with Kawasaki disease & MIS-C.
The Journal of Clinical Investigation 2021; 131(20):e147076. PMID: 34464357.
IVIG targets IL-1b+ neutrophils via non-apoptotic cell death Immune response to intravenous immunoglobulin in patients with Kawasaki disease and MIS-C. 

b-glucan dependent shuttling of conidia from neutrophils to macrophages occurs during fungal infection establishment. 
PLoS Biol 2019,

Research Activities

We are an inflammation laboratory with a broad interest in the intersection of cell death, neutrophil biology, and innate immunity. Here are some of our recent research programs which seek to understand the pathophysiology of human inflammatory diseases:
  1. We identified roles for the MLKL-dependent cell death pathway in neutrophil extracellular trap formation. PAD4 is activated downstream of MLKL, and was essential for generation of NETs but surprisingly was not required for chromatin decondensation. This work has revealed a novel signaling pathway controlled by MLKL. Parallel studies of GSDMD-dependent NET formation and non-canonical inflammasome activation provides a genetic framework to explore the relationship between non-apoptotic neutrophil cell death, NET generation, and responses to infection.
  2. We identified a novel Ptpn6 Y208N mutant mouse strain causing cutaneous inflammation of the feet. Mice carrying neutrophil-specific deletions of Ptpn6 develop neutrophilic dermatoses caused by MLKL- and Caspase-8-dependent inflammatory cell death driving IL-1 release.
  3. Our laboratory identified a novel phenomena called shuttling in mammalian cells, which involves the transfer of intracellular fungal pathogens from neutrophils to macrophages. 
  4. clinical study of patients with Kawasaki disease and the COVID-19-associated multisystem inflammatory syndrome in children (MIS-C) identified IL-1b+ neutrophils as a key immune cell targeted by intravenous immunoglobulin using a novel cell death pathway dependent on PI3-kinase and NADPH oxidase. 

Techniques/Expertise

Neutrophils, Macrophages, Hematopoietic Stem Cells, Cell Death, Inflammation, Innate Immunity

Disease Models

Inflammasomopathies, MIS-C, COVID-19, Neutrophilic dermatoses

Genetically Modified Organisms

NLRP3, Dectin-1, Mlkl, PAD4

Research Images

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Upcoming Events

  • Feb 15

    Lorne Infection and Immunity Conference 2023

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  • Feb 15

    Lorne Infection and Immunity Conference 2023

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