Evidence map›Paper›PMID 29254755›Full record

ReviewSeminars in immunology2018

Human genetics of infectious diseases: Unique insights into immunological redundancy.

Jean-Laurent Casanova, Laurent Abel

Abstract readReview
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed.

  1. Review
  2. Review
  3. Commentary: A rare case report ofFrontiers in pediatrics · 2026
    Article
  4. Article
  5. Article
  6. Human immunity.Journal of human immunity · 2025
    Article
  7. Article
  8. The monogenic landscape of human infectious diseases.The Journal of allergy and clinical immunology · 2025
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Jean-Laurent CasanovaSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA; Howard Hughes Medical Institute, New York, NY, USA; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, Inserm U1163, Necker Hospital for Sick Children, Paris, France, EU; Paris Descartes University, Imagine Institute, Paris, France, EU; Pediatric Hematology and Immunology Unit, Necker Hospital for Sick Children, Paris, France, EU. Electronic address: casanova@rockefeller.edu.
Laurent AbelSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA; Laboratory of Human Genetics of Infectious Diseases, Necker Branch, Inserm U1163, Necker Hospital for Sick Children, Paris, France, EU; Paris Descartes University, Imagine Institute, Paris, France, EU. Electronic address: laurent.abel@inserm.fr.

Funding

Developing, Demonstrating, and Disseminating Innovative Programs to Achieve Translational SuccessUL1TR001866 · NCATS · ROCKEFELLER UNIVERSITY · PI COLLER, BARRY, KRUEGER, JAMES G · 2016 to 2025
$40.6M
Regulation of IgA class switching in the intestinal mucosaP01AI061093 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CASANOVA, JEAN-LAURENT · 2004 to 2021
$29.8M
Study of the Cellular Basis of Herpes Simplex Encephalitis with hPSC-Derived CNS and PNS CellsR01NS072381 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI Jean-Laurent Casanova, Shen-Ying Zhang · 2010 to 2026
$10.2M
Monogenic basis of resistance to SARS-CoV2 and predisposition to severe COVID-19R01AI088364 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Jean-Laurent Casanova, Shen-Ying Zhang · 2010 to 2026
$8.7M
Genome-wide search for inborn errors of IL-17 immunity underlying chronic mucocutaneous candidiasisR01AI127564 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI Jean-Laurent Casanova · 2017 to 2026
$4.8M
Genome-Wide Dissection of Mendelian Susceptibility to Mycobacterial DiseaseR37AI095983 · NIAID · ROCKEFELLER UNIVERSITY · PI CASANOVA, JEAN-LAURENT · 2011 to 2020
$4.6M
A genetic dissection of Mendelian susceptibility to mycobacterial diseases (MSMD)R01AI089970 · NIAID · ROCKEFELLER UNIVERSITY · PI CASANOVA, JEAN-LAURENT · 2010 to 2014
$2.5M
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR001866NIAID NIH HHS P01 AI061093NIAID NIH HHS R01 AI088364NIAID NIH HHS R01 AI089970NIAID NIH HHS R01 AI127564NIAID NIH HHS R37 AI095983NINDS NIH HHS R01 NS072381
6 · The paper itself

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.

Indexed as

GenotypeAsymptomatic DiseasesBiological EvolutionCommunicable DiseasesGenetic Diseases, X-LinkedGenetic Predisposition to DiseaseHost-Pathogen InteractionsHumansImmunityImmunologic Deficiency SyndromesPhenotypeViral TropismInborn error of immunityKnockoutLoss of functionNatural selectionPrimary infectionRedundancy

Identifiers

PMID29254755
PMCPMC5910248

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.