Format

Send to

Choose Destination
Proc Natl Acad Sci U S A. 1999 Mar 2;96(5):2250-5.

Innate and acquired humoral immunities to influenza virus are mediated by distinct arms of the immune system.

Author information

1
Department of Genetics, Stanford University Medical School, Stanford, CA 94305, USA. Baumgarth@Stanford.edu

Abstract

"Natural" Igs, mainly IgM, comprise part of the innate immune system present in healthy individuals, including antigen-free mice. These Igs are thought to delay pathogenicity of infecting agents until antigen-induced high affinity Igs of all isotypes are produced. Previous studies suggested that the acquired humoral response arises directly from the innate response, i.e., that B cells expressing natural IgM, upon antigen encounter, differentiate to give rise both to cells that secrete high amounts of IgM and to cells that undergo affinity maturation and isotype switching. However, by using a murine model of influenza virus infection, we demonstrate here that the B cells that produce natural antiviral IgM neither increase their IgM production nor undergo isotype switching to IgG2a in response to the infection. These cells are distinct from the B cells that produce the antiviral response after encounter with the pathogen. Our data therefore demonstrate that the innate and the acquired humoral immunities to influenza virus are separate effector arms of the immune system and that antigen exposure per se is not sufficient to increase natural antibody production.

PMID:
10051627
PMCID:
PMC26769
DOI:
10.1073/pnas.96.5.2250
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center