期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 219, 期 4, 页码 -出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20211387
关键词
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资金
- Howard Hughes Medical Institute
- Rockefeller University
- St. Giles Foundation
- National Institutes of Health [R01AI088364, R01AI095983, R01AI127564, R01AI163029]
- National Center for Advancing Translational Sciences
- National Institutes of Health Clinical and Translational Science Awards program [UL1 TR001866]
- Fisher Center for Alzheimer's Research Foundation
- Meyer Foundation
- JPB Foundation
- French National Research Agency (ANR) under the Investments for the Future program [ANR-10-IAHU-01]
- Integrative Biology of Emerging Infectious Diseases Laboratory of Excellence [ANR-10-LABX-62IBEID]
- French Foundation for Medical Research [EQU201903007798]
- Agence nationale de recherches sur le sida et les hepatites virales Nord-Sud [ANRS-COV05]
- ANR GENVIR [ANR-20-CE93-003]
- ANR AABIFNCOV [ANR-20CO11-0001]
- ANR GenMIS-C [ANR-21-COVR-0039]
- ECOS-Nord [C19S0163407]
- European Union [824110]
- Square Foundation
- Grandir-Fonds de solidarite pour l'Enfance
- Fondation du Souffle
- SCOR Corporate Foundation for Science
- Institut National de la Sante et de la Recherche Medicale (INSERM)
- French Ministry of Higher Education, Research, and Innovation (MESRI-COVID-19)
- REACTing-INSERM
- University of Paris
- Fondation Recherche Medicale [EA20170638020]
- MD-PhD program of the Imagine Institute
- Fondation Bettencourt Schueller
- Agence Nationale de la Recherche (ANR) [ANR-21-COVR-0039] Funding Source: Agence Nationale de la Recherche (ANR)
The vast clinical variability in microbial infections can be explained by human genetic and immunological factors, with autoantibodies playing a role in specific infectious diseases.
The vast interindividual clinical variability observed in any microbial infection-ranging from silent infection to lethal disease-is increasingly being explained by human genetic and immunological determinants. Autoantibodies neutralizing specific cytokines underlie the same infectious diseases as inborn errors of the corresponding cytokine or response pathway. Autoantibodies against type I IFNs underlie COVID-19 pneumonia and adverse reactions to the live attenuated yellow fever virus vaccine. Autoantibodies against type II IFN underlie severe disease caused by environmental or tuberculous mycobacteria, and other intra-macrophagic microbes. Autoantibodies against IL-17A/F and IL-6 are less common and underlie mucocutaneous candidiasis and staphylococcal diseases, respectively. Inborn errors of and autoantibodies against GM-CSF underlie pulmonary alveolar proteinosis; associated infections are less well characterized. In individual patients, autoantibodies against cytokines preexist infection with the pathogen concerned and underlie the infectious disease. Human antibody-driven autoimmunity can interfere with cytokines that are essential for protective immunity to specific infectious agents but that are otherwise redundant, thereby underlying specific infectious diseases.
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