Journal
JOURNAL OF CLINICAL IMMUNOLOGY
Volume 34, Issue -, Pages S30-S34Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10875-014-0017-4
Keywords
TRIM21; neutralization; antiviral
Categories
Funding
- Medical Research Council [MC_U105181010] Funding Source: researchfish
- MRC [MC_U105181010] Funding Source: UKRI
- Medical Research Council [MC_U105181010] Funding Source: Medline
Ask authors/readers for more resources
Antibodies allow the immune system to target pathogens despite their tremendous diversity and rapid evolution. Once bound to a pathogen, antibodies induce a broad range of effector mechanisms, including phagocytosis and complement. However, these mechanisms are all initiated in the extracellular space, meaning that pathogens like viruses evade them upon infection of their target cells. Recently, it has been shown that, in addition to mediating extracellular immune responses, antibodies also activate immunity inside infected cells. Antibodies that are bound to the surface of non-enveloped viruses or bacteria are carried into the cell during pathogen entry. Once inside the cell, these pathogen-attached antibodies are recognised by a highly conserved, high affinity cytosolic antibody receptor called TRIM21. TRIM21 initiates both sensor and effector responses that reduce viral replication and induce an antiviral state. These responses are an important part of antiviral immunity and the removal of TRIM21 results in uncontrolled viraemia and death in a mouse model of infection.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available