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Malar J. 2016 Mar 3;15:139. doi: 10.1186/s12936-016-1190-0.

B cell sub-types following acute malaria and associations with clinical immunity.

Author information

1
Department of Medicine, University of California San Francisco, Box 0811, San Francisco, CA, 94110, USA. Richard.Sullivan@UCSF.edu.
2
Infectious Disease Research Collaboration, Tororo, Uganda. sewyisaac@yahoo.co.uk.
3
Department of Immunology and Infection, London School of Hygiene and Tropical Medicine, London, UK. sewyisaac@yahoo.co.uk.
4
Infectious Disease Research Collaboration, Tororo, Uganda. wamalasamuel@gmail.com.
5
Infectious Disease Research Collaboration, Tororo, Uganda. nankyafelistas@gmail.com.
6
Department of Medicine, University of California San Francisco, Box 0811, San Francisco, CA, 94110, USA. prasannaj@gmail.com.
7
Centers for Disease Control and Prevention, Atlanta, GA, USA. jwt0@cdc.gov.
8
Infectious Disease Research Collaboration, Tororo, Uganda. hmk@chs.mak.ac.ug.
9
Makerere University Medical School, Kampala, Uganda. hmk@chs.mak.ac.ug.
10
Infectious Disease Research Collaboration, Tororo, Uganda. marymkakuru@gmail.com.
11
Infectious Disease Research Collaboration, Tororo, Uganda. earinaitwe@idrc-uganda.org.
12
Infectious Disease Research Collaboration, Tororo, Uganda. mkamya@idrc-uganda.org.
13
Makerere University Medical School, Kampala, Uganda. mkamya@idrc-uganda.org.
14
Department of Medicine, University of California San Francisco, Box 0811, San Francisco, CA, 94110, USA. grant.dorsey@ucsf.edu.
15
Department of Medicine, University of California San Francisco, Box 0811, San Francisco, CA, 94110, USA. Margaret.Feeney@ucsf.edu.
16
Department of Immunology and Infection, London School of Hygiene and Tropical Medicine, London, UK. Eleanor.Riley@lshtm.ac.uk.
17
Department of Immunology and Infection, London School of Hygiene and Tropical Medicine, London, UK. Chris.Drakeley@lshtm.ac.uk.
18
Department of Medicine, University of California San Francisco, Box 0811, San Francisco, CA, 94110, USA. bgreenhouse@medsfgh.ucsf.edu.
19
Department of Medicine, University of California San Francisco, Box 0811, San Francisco, CA, 94110, USA. richard.sullivan@ucsf.edu.

Abstract

BACKGROUND:

Repeated exposure to Plasmodium falciparum is associated with perturbations in B cell sub-set homeostasis, including expansion atypical memory B cells. However, B cell perturbations immediately following acute malaria infection have been poorly characterized, especially with regard to their relationship with immunity to malaria.

METHODS:

To better understand the kinetics of B cell sub-sets following malaria, the proportions of six B cell sub-sets were assessed at five time points following acute malaria in four to 5 years old children living in a high transmission region of Uganda. B cell sub-set kinetics were compared with measures of clinical immunity to malaria-lower parasite density at the time of malaria diagnosis and recent asymptomatic parasitaemia.

RESULTS:

Atypical memory B cell and transitional B cell proportions increased following malaria. In contrast, plasmablast proportions were highest at the time of malaria diagnosis and rapidly declined following treatment. Increased proportions of atypical memory B cells were associated with greater immunity to malaria, whereas increased proportions of transitional B cells were associated with evidence of less immunity to malaria.

CONCLUSIONS:

These findings highlight the dynamic changes in multiple B cell sub-sets following acute, uncomplicated malaria, and how these sub-sets are associated with developing immunity to malaria.

PMID:
26939776
PMCID:
PMC4778296
DOI:
10.1186/s12936-016-1190-0
[Indexed for MEDLINE]
Free PMC Article

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