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Gonzales SJ, Bol S, Braddom AE, et al. Longitudinal analysis of FcRL5 expression and clonal relationships among classical and atypical memory B cells following malaria. Malar J. 2021;20(1):435doi: 10.1186/s12936-021-03970-1.
Gonzales, S. J., Bol, S., Braddom, A. E., Sullivan, R., Reyes, R. A., Ssewanyana, I., Eggers, E., Greenhouse, B., & Bunnik, E. M. (2021). Longitudinal analysis of FcRL5 expression and clonal relationships among classical and atypical memory B cells following malaria. Malaria journal, 20(1), 435. https://doi.org/10.1186/s12936-021-03970-1
Gonzales, S Jake, et al. "Longitudinal analysis of FcRL5 expression and clonal relationships among classical and atypical memory B cells following malaria." Malaria journal vol. 20,1 (2021): 435. doi: https://doi.org/10.1186/s12936-021-03970-1
Gonzales SJ, Bol S, Braddom AE, Sullivan R, Reyes RA, Ssewanyana I, Eggers E, Greenhouse B, Bunnik EM. Longitudinal analysis of FcRL5 expression and clonal relationships among classical and atypical memory B cells following malaria. Malar J. 2021 Nov 10;20(1):435. doi: 10.1186/s12936-021-03970-1. PMID: 34758841; PMCID: PMC8579674.
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Malar J. 2021 Nov 10;20(1):435. doi: 10.1186/s12936-021-03970-1.

Longitudinal analysis of FcRL5 expression and clonal relationships among classical and atypical memory B cells following malaria.

Malaria journal

S Jake Gonzales, Sebastiaan Bol, Ashley E Braddom, Richard Sullivan, Raphael A Reyes, Isaac Ssewanyana, Erica Eggers, Bryan Greenhouse, Evelien M Bunnik

Affiliations

  1. Department of Microbiology, Immunology and Molecular Genetics, Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
  2. Department of Medicine, University of California San Francisco, San Francisco, CA, USA.
  3. Shape Therapeutics, 219 Terry St., Seattle, WA, USA.
  4. London School of Hygiene and Tropical Medicine, London, UK.
  5. Infectious Disease Research Collaboration, Kampala, Uganda.
  6. Department of Neurology, UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, CA, USA.
  7. Department of Microbiology, Immunology and Molecular Genetics, Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA. [email protected].

PMID: 34758841 PMCID: PMC8579674 DOI: 10.1186/s12936-021-03970-1

Abstract

BACKGROUND: Chronic and frequently recurring infectious diseases, such as malaria, are associated with expanded populations of atypical memory B cells (MBCs). These cells are different from classical MBCs by the lack of surface markers CD21 and CD27 and increased expression of inhibitory receptors, such as FcRL5. While the phenotype and conditions leading to neogenesis of atypical MBCs in malaria-experienced individuals have been studied extensively, the origin of these cells remains equivocal. Functional similarities between FcRL5

METHODS: Here, a longitudinal analysis of FcRL5 expression in various B cell subsets was performed in two children from a high transmission region in Uganda over a 6-month period in which both children experienced a malaria episode. Using B-cell receptor (BCR)-sequencing to track clonally related cells, the connections between IgM

RESULTS: The highest expression of FcRL5 was found among IgG

CONCLUSIONS: Collectively, these results suggest fundamental differences between unswitched and class-switched B cell populations and provide clues about the primary developmental pathways of atypical MBCs in malaria-experienced individuals.

© 2021. The Author(s).

Keywords: Adaptive immune response; B cell differentiation; B cell receptor; BCR-sequencing; Humoral immunity; Infection; Plasmodium falciparum

References

  1. PLoS Pathog. 2017 Sep 27;13(9):e1006576 - PubMed
  2. J Immunol. 2009 Aug 1;183(3):2176-82 - PubMed
  3. J Infect Dis. 2015 Nov 1;212(9):1429-38 - PubMed
  4. PLoS Pathog. 2015 May 19;11(5):e1004894 - PubMed
  5. Clin Microbiol Rev. 2009 Jan;22(1):13-36, Table of Contents - PubMed
  6. Nat Commun. 2018 May 1;9(1):1758 - PubMed
  7. Front Immunol. 2017 Aug 21;8:966 - PubMed
  8. Philos Trans R Soc Lond B Biol Sci. 2015 Sep 5;370(1676): - PubMed
  9. PLoS Pathog. 2010 May 20;6(5):e1000912 - PubMed
  10. Nat Med. 2020 Dec;26(12):1929-1940 - PubMed
  11. Nat Immunol. 2015 Jul;16(7):755-65 - PubMed
  12. Nat Biotechnol. 2017 Sep;35(9):879-884 - PubMed
  13. Immunity. 2015 Mar 17;42(3):580-90 - PubMed
  14. Cell Rep. 2021 Feb 9;34(6):108684 - PubMed
  15. Immunity. 2019 Aug 20;51(2):398-410.e5 - PubMed
  16. Eur J Immunol. 2020 Aug;50(8):1187-1194 - PubMed
  17. Nat Methods. 2015 May;12(5):380-1 - PubMed
  18. Elife. 2015 May 08;4: - PubMed
  19. Front Immunol. 2019 Apr 24;10:852 - PubMed
  20. Int J Parasitol. 2020 Nov;50(13):1033-1042 - PubMed
  21. J Exp Med. 2013 Feb 11;210(2):389-99 - PubMed
  22. BMC Med. 2014 Jul 01;12:108 - PubMed
  23. JCI Insight. 2019 Apr 2;5: - PubMed
  24. Proc Natl Acad Sci U S A. 2010 Apr 13;107(15):6958-63 - PubMed
  25. Nat Biotechnol. 2012 May;30(5):434-9 - PubMed
  26. Cell Rep. 2019 Apr 30;27(5):1446-1460.e4 - PubMed
  27. Elife. 2019 May 15;8: - PubMed
  28. PLoS Med. 2010 Jan 19;7(1):e1000218 - PubMed
  29. Nat Immunol. 2008 Jul;9(7):725-32 - PubMed
  30. Am J Trop Med Hyg. 2015 May;92(5):903-12 - PubMed
  31. J Exp Med. 2008 Aug 4;205(8):1797-805 - PubMed
  32. JCI Insight. 2017 Nov 16;2(22): - PubMed
  33. J Exp Med. 2021 Apr 5;218(4): - PubMed
  34. Proc Natl Acad Sci U S A. 2007 Jun 5;104(23):9770-5 - PubMed
  35. Sci Adv. 2020 Jul 24;6(30):eaba6493 - PubMed

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