ReviewSeminars in immunology2018
Human genetics of infectious diseases: Unique insights into immunological redundancy.
Review in Seminars in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed.
- Toward a monogenic architecture of human infections: From 1996 to 2026.Journal of human immunity · 2026Review
- Forging resilient warriors within: exercise's epic role in training innate immunity and taming inflammation's storm.Frontiers in immunology · 2026Review
- Commentary: A rare case report ofFrontiers in pediatrics · 2026Article
- MAGIS syndrome: phenotypes, pathogenesis, and treatment.Journal of human immunity · 2025Article
- Genetic landscape of Romanian children with inborn errors of immunity via gene panels, exome, and genome sequencing.Scientific reports · 2025Article
- Human immunity.Journal of human immunity · 2025Article
- Human inborn errors of immunity: 2024 update on the classification from the International Union of Immunological Societies Expert Committee.Journal of human immunity · 2025Article
- The monogenic landscape of human infectious diseases.The Journal of allergy and clinical immunology · 2025Review
- Understanding Heritable Variation Among Hosts in Infectious Diseases Through the Lens of Twin Studies.Genes · 2025Review
- Insights into the genetic theory of infectious diseases.La Tunisie medicale · 2024Review
- Type I interferon pathway genetic variants in severe COVID-19.Virus research · 2024Review
- Interferons-Implications in the Immune Response to Respiratory Viruses.Microorganisms · 2023Review
- Encephalitis and poor neuronal death-mediated control of herpes simplex virus in human inherited RIPK3 deficiency.Science immunology · 2023Article
- Impact of SARS-CoV-2 infection and COVID-19 on patients with inborn errors of immunity.The Journal of allergy and clinical immunology · 2023Review
- Inborn Errors of Immunity Predisposing to Herpes Simplex Virus Infections of the Central Nervous System.Pathogens (Basel, Switzerland) · 2023Review
- Mannose-binding lectin gene polymorphism in psoriasis and vitiligo: an observational study and computational analysis.Frontiers in medicine · 2023Article
- Anxiety, depression, and memory loss in Chagas disease: a puzzle far beyond neuroinflammation to be unpicked and solved.Memorias do Instituto Oswaldo Cruz · 2023Article
- Impaired IL-23-dependent induction of IFN-γ underlies mycobacterial disease in patients with inherited TYK2 deficiency.The Journal of experimental medicine · 2022Article
- Human Inborn Errors of Immunity: 2022 Update on the Classification from the International Union of Immunological Societies Expert Committee.Journal of clinical immunology · 2022Article
- Integrative genetic and immune cell analysis of plasma proteins in healthy donors identifies novel associations involving primary immune deficiency genes.Genome medicine · 2022Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors.
Funding
Abstract
For almost any given human-tropic virus, bacterium, fungus, or parasite, the clinical outcome of primary infection is enormously variable, ranging from asymptomatic to lethal infection. This variability has long been thought to be largely determined by the germline genetics of the human host, and this is increasingly being demonstrated to be the case. The number and diversity of known inborn errors of immunity is continually increasing, and we focus here on autosomal and X-linked recessive traits underlying complete deficiencies of the encoded protein. Schematically, four types of infectious phenotype have been observed in individuals with such deficiencies, each providing information about the redundancy of the corresponding human gene, in terms of host defense in natural conditions. The lack of a protein can confer vulnerability to a broad range of microbes in most, if not all patients, through the disruption of a key immunological component. In such cases, the gene concerned is of low redundancy. However, the lack of a protein may also confer vulnerability to a narrow range of microbes, sometimes a single pathogen, and not necessarily in all patients. In such cases, the gene concerned is highly redundant. Conversely, the deficiency may be apparently neutral, conferring no detectable predisposition to infection in any individual. In such cases, the gene concerned is completely redundant. Finally, the lack of a protein may, paradoxically, be advantageous to the host, conferring resistance to one or more infections. In such cases, the gene is considered to display beneficial redundancy. These findings reflect the current state of evolution of humans and microbes, and should not be considered predictive of redundancy, or of a lack of redundancy, in the distant future. Nevertheless, these observations are of potential interest to present-day biologists testing immunological hypotheses experimentally and physicians managing patients with immunological or infectious conditions.
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