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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2250-2255 |
| Number of pages | 6 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Volume | 96 |
| Issue number | 5 |
| DOIs | |
| State | Published - Mar 2 1999 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Genetics
- General
Cite this
Innate and acquired humoral immunities to influenza virus are mediated by distinct arms of the immune system. / Baumgarth, Nicole; Herman, Ometa C.; Jager, Gina C.; Brown, Lorena; Herzenberg, Leonard A.; Herzenberg, Leonore A.
In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 96, No. 5, 02.03.1999, p. 2250-2255.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Innate and acquired humoral immunities to influenza virus are mediated by distinct arms of the immune system
AU - Baumgarth, Nicole
AU - Herman, Ometa C.
AU - Jager, Gina C.
AU - Brown, Lorena
AU - Herzenberg, Leonard A.
AU - Herzenberg, Leonore A.
PY - 1999/3/2
Y1 - 1999/3/2
N2 - '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.
AB - '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.
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UR - http://www.scopus.com/inward/citedby.url?scp=0033515101&partnerID=8YFLogxK
U2 - 10.1073/pnas.96.5.2250
DO - 10.1073/pnas.96.5.2250
M3 - Article
C2 - 10051627
AN - SCOPUS:0033515101
VL - 96
SP - 2250
EP - 2255
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 5
ER -