Atypical and classical memory B cells produce Plasmodium falciparum neutralizing antibodies
Research output: Contribution to journal › Journal article › Research › peer-review
Standard
Atypical and classical memory B cells produce Plasmodium falciparum neutralizing antibodies. / Muellenbeck, Matthias F; Ueberheide, Beatrix; Amulic, Borko; Epp, Alexandra; Fenyo, David; Busse, Christian E; Esen, Meral; Theisen, Michael; Mordmüller, Benjamin; Wardemann, Hedda.
In: Journal of Experimental Medicine, Vol. 210, No. 2, 11.02.2013, p. 389-99.Research output: Contribution to journal › Journal article › Research › peer-review
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Atypical and classical memory B cells produce Plasmodium falciparum neutralizing antibodies
AU - Muellenbeck, Matthias F
AU - Ueberheide, Beatrix
AU - Amulic, Borko
AU - Epp, Alexandra
AU - Fenyo, David
AU - Busse, Christian E
AU - Esen, Meral
AU - Theisen, Michael
AU - Mordmüller, Benjamin
AU - Wardemann, Hedda
PY - 2013/2/11
Y1 - 2013/2/11
N2 - Antibodies can protect from Plasmodium falciparum (Pf) infection and clinical malaria disease. However, in the absence of constant reexposure, serum immunoglobulin (Ig) levels rapidly decline and full protection from clinical symptoms is lost, suggesting that B cell memory is functionally impaired. We show at the single cell level that natural Pf infection induces the development of classical memory B cells (CM) and atypical memory B cells (AtM) that produce broadly neutralizing antibodies against blood stage Pf parasites. CM and AtM contribute to anti-Pf serum IgG production, but only AtM show signs of active antibody secretion. AtM and CM were also different in their IgG gene repertoire, suggesting that they develop from different precursors. The findings provide direct evidence that natural Pf infection leads to the development of protective memory B cell antibody responses and suggest that constant immune activation rather than impaired memory function leads to the accumulation of AtM in malaria. Understanding the memory B cell response to natural Pf infection may be key to the development of a malaria vaccine that induces long-lived protection.
AB - Antibodies can protect from Plasmodium falciparum (Pf) infection and clinical malaria disease. However, in the absence of constant reexposure, serum immunoglobulin (Ig) levels rapidly decline and full protection from clinical symptoms is lost, suggesting that B cell memory is functionally impaired. We show at the single cell level that natural Pf infection induces the development of classical memory B cells (CM) and atypical memory B cells (AtM) that produce broadly neutralizing antibodies against blood stage Pf parasites. CM and AtM contribute to anti-Pf serum IgG production, but only AtM show signs of active antibody secretion. AtM and CM were also different in their IgG gene repertoire, suggesting that they develop from different precursors. The findings provide direct evidence that natural Pf infection leads to the development of protective memory B cell antibody responses and suggest that constant immune activation rather than impaired memory function leads to the accumulation of AtM in malaria. Understanding the memory B cell response to natural Pf infection may be key to the development of a malaria vaccine that induces long-lived protection.
U2 - 10.1084/jem.20121970
DO - 10.1084/jem.20121970
M3 - Journal article
C2 - 23319701
VL - 210
SP - 389
EP - 399
JO - The Journal of Experimental Medicine
JF - The Journal of Experimental Medicine
SN - 0022-1007
IS - 2
ER -
ID: 45049251