The human model: a genetic dissection of immunity to infection in natural conditions View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2004-01

AUTHORS

Jean-Laurent Casanova, Laurent Abel

ABSTRACT

Key PointsInfection and immunity in humans occur in natural conditions, as opposed to experimental conditions in animal models. In our view, this accounts for most of the advantages and disadvantages of human studies, when compared with animal studies.Immunocompetence can be defined as the immune status that results in self-healing infection, with or without symptoms, but of favourable outcome without any specific treatment. After exposure to the microbial world, human immunocompetence (to all microorganisms) is rare and immunodeficiency (to at least one microorganism) is, therefore, the rule rather than the exception.All clinical and biological phenotypes in the course of an infectious disease result from the complex interaction between environmental (microbial and non-microbial) and host (genetic and non-genetic) factors. A forward-genetic dissection of immunity to infection is therefore possible.The human model is an indispensable complement to animal studies, as it provides insight into the ecologically relevant and evolutionary selected functions of cells and molecules that are involved in immunity to infection. The forward-genetic dissection of immunity to infection in humans benefits from being an observational study of host–environment interaction in a natural ecosystem.In some cases, 'wild-type' individuals are vulnerable to common infection, whereas mutants with relatively common Mendelian mutations are fully resistant and otherwise healthy. Examples include resistance to Plasmodium vivax associated with recessive mutations in Duffy antigen receptor for chemokines (DARC), resistance to HIV-1 with recessive mutations in CC-chemokine receptor 5 (CCR5) and resistance to noroviruses with recessive mutations in fucosyltransferase 2 (FUT2).Studies of human genetics of infectious diseases have challenged several immunological theories and, to a lesser extent, data obtained in mice. Examples include the lack of viral diseases in children with mutations that impair antigen presentation to, or recognition by, cytotoxic CD8+ T cells, and the narrow spectrum of infections in children with mutations in the interleukin-12 (IL-12)–interferon-γ pathway or IL-1 receptor-associated kinase 4 (IRAK4).The study of Mendelian 'holes' in immunity to infection has indicated the existence of 'pathogen-specific' genes in natural conditions of infection. Examples include the group of genetic defects of the terminal components of complement, associated with Neisseria infections, and epidermodysplasia verruciformis, associated with a selective susceptibility to human papillomaviruses.There is a continuous spectrum between rare Mendelian vulnerability to poorly virulent microorganisms and common complex predisposition to virulent microorganisms. The elucidation of the genetic basis of common infectious diseases also sheds light on immunological mechanisms. Mendelian susceptibility to tuberculosis and complex susceptibility to leprosy have indicated the function of important immunological pathways. More... »

PAGES

55-66

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    DOI

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    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/14704768


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