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Cited by 31Immunodeficiency and Autoimmune DisordersT-cell and B-cell ImmunologyChemokine receptors and signaling

Migration-induced cell shattering due to DOCK8 deficiency causes a type 2–biased helper T cell response

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Schneider, Caitlin, Shen, Connie, Gopal, Angelica A., Douglas, Todd, Forestell, Benjamin, Kauffman, Keith D., Rogers, Dakota, Artusa, Patricio +9 more·2020·Nature Immunology
DOI 10.1038/s41590-020-0795-1PMC PMC10478007
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Abstract

Mutations that impact immune cell migration and result in immune deficiency illustrate the importance of cell movement in host defense. In humans, loss-of-function mutations in DOCK8, a guanine exchange factor involved in hematopoietic cell migration, lead to immunodeficiency and, paradoxically, allergic disease. Here, we demonstrate that, like humans, Dock8-/- mice have a profound type 2 CD4+ helper T (T H 2) cell bias upon pulmonary infection with Cryptococcus neoformans and other non-T H 2 stimuli. We found that recruited Dock8-/-CX3CR1+ mononuclear phagocytes are exquisitely sensitive to migration-induced cell shattering, releasing interleukin (IL)-1β that drives granulocyte-macrophage colony-stimulating factor (GM-CSF) production by CD4+ T cells. Blocking IL-1β, GM-CSF or caspase activation eliminated the type-2 skew in mice lacking Dock8. Notably, treatment of infected wild-type mice with apoptotic cells significantly increased GM-CSF production and T H 2 cell differentiation. This reveals an important role for cell death in driving type 2 signals during infection, which may have implications for understanding the etiology of type 2 CD4+ T cell responses in allergic disease.

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Authors
Schneider, C., Shen, C., Gopal, A. A., Douglas, T., Forestell, B., Kauffman, K. D., Rogers, D., Artusa, P., Zhang, Q., Jing, H., Freeman, A. F., Barber, D. L., King, I. L., Saleh, M., Wiseman, P. W., Su, H. C., & Mandl, J. N.
Affiliations
  • McGill University (CA)
  • Massachusetts General Hospital (US)
  • National Institutes of Health (US)
  • McGill University Health Centre (CA)
  • Université de Bordeaux (FR)
Corresponding author
Mandl, Judith N.
ORCID
Venue
Nature Immunology
Publisher
Springer Science and Business Media LLC
Published
2020-10-05
Volume
21
Issue
12
Pages
1528-1539
ISSN
  • 1529-2908 (ISSN-L)
  • 1529-2916
DOI
10.1038/s41590-020-0795-1
PMC
PMC10478007
OpenAlex
W3089587040
Cited by
31
References
6
Citations by year
2026: 2 · 2025: 6 · 2024: 6 · 2023: 4 · 2022: 4 · 2021: 7 · 2020: 2
FWCI
1.46
Type
journal article
Language
en
Open access
Licence
Locations
  • Nature Immunology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • University of Pennsylvania
  • McGill University
  • Kenneth Rainin Foundation (KRA000021)
  • Sidra Medicine
  • National Institutes of Health
  • Canadian Institutes of Health Research (201603PJT)
  • Natural Sciences and Engineering Research Council of Canada
  • National Institute of Allergy and Infectious Diseases (ZIAAI001193)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immunodeficiency and Autoimmune Disorders
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
Keywords
DOCK8, leukocyte migration, Th2 cells, Cryptococcus neoformans, pulmonary infection, IL-1β, GM-CSF, caspase activation, apoptotic cells, allergic diseases, immunodeficiency, guanine nucleotide exchange factor
MeSH terms
Animals, Cell Movement, Disease Susceptibility, Humans, Leukocytes, Mononuclear, Lymphocyte Activation, Phagocytes, Signal Transduction, Biomarkers, Gene Expression, Immunophenotyping, Granulocyte-Macrophage Colony-Stimulating Factor, Cytokines, Mice, Knockout, Th2 Cells, Caspases, Guanine Nucleotide Exchange Factors, Myeloid Cells, Mice

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