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Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
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Among the three main modes of HGT—transformation, conjugation, and transduction—transduction is unique in that it is mediated by bacteriophages, or bacterial viruses.Transduction occurs in two ways. Generalized transduction occurs during the lytic cycle of a bacteriophage infection. In this process, bacteriophages infect bacterial cells, replicate within them, and ultimately cause cell lysis, releasing newly assembled virions. Occasionally, random fragments of the bacterial genome...
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Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
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Related Experiment Video

Updated: Nov 2, 2025

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TNFRSF13B polymorphisms counter microbial adaptation to enteric IgA.

Jeffrey L Platt1, Mayara Garcia de Mattos Barbosa2, Daniel Huynh2

  • 1Department of Microbiology and Immunology and Department of Surgery.

JCI Insight
|June 10, 2021
PubMed
Summary

Common genetic variants in TNFRSF13B (transmembrane activator and CAML interactor) offer resistance to gut pathogens. This resistance is linked to IgA deficiency and suggests balancing selection maintains these variants.

Keywords:
Bacterial infectionsGenetic variationImmunoglobulinsImmunologyMicrobiology

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Area of Science:

  • Immunology
  • Genetics
  • Microbiology

Background:

  • TNFRSF13B (transmembrane activator and CAML interactor) encodes a receptor crucial for plasma cell differentiation and host defense.
  • Dominant-negative TNFRSF13B alleles are common but rarely cause disease, suggesting a potential selective advantage.
  • Enteric pathogens pose a significant threat, and understanding host resistance mechanisms is vital.

Purpose of the Study:

  • To investigate the hypothesis that loss-of-function TNFRSF13B variants confer resistance to enteric pathogens.
  • To elucidate the mechanism by which a common human variant (TNFRSF13B A181E) impacts host defense against Citrobacter rodentium.

Main Methods:

  • Generated mice with engineered tnfrsf13b variants analogous to the human A181E mutation.
  • Assessed resistance to Citrobacter rodentium infection and transmission in these engineered mice.
  • Investigated the role of intestinal immunoglobulin A (IgA) in pathogen virulence and host defense.

Main Results:

  • Engineered mice exhibited significant resistance to Citrobacter rodentium pathogenicity and transmission.
  • This resistance was primarily attributed to natural IgA deficiency in the engineered mice's intestines.
  • In the presence of IgA, enteric pathogens like C. rodentium can hijack antibody binding to induce virulence gene expression.

Conclusions:

  • Enteric pathogens have evolved to exploit host antibodies (IgA) to trigger their virulence factors.
  • The high frequency of dominant-negative TNFRSF13B variants is likely a result of balancing selection, providing an advantage against certain infections.
  • This study reveals a novel mechanism of host-pathogen interaction and explains the evolutionary persistence of specific genetic variants.