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The survival of B cells is compromised in kidney disease

Author

Listed:
  • Doureradjou Peroumal

    (University of Pittsburgh
    University of Pittsburgh)

  • Chetan V. Jawale

    (University of Pittsburgh
    University of Pittsburgh)

  • Wonseok Choi

    (University of Pittsburgh
    University of Pittsburgh
    Stony Brook University)

  • Hossein Rahimi

    (University of Pittsburgh
    University of Pittsburgh
    Stony Brook University)

  • Danielle Antos

    (University of Pittsburgh
    University of Pittsburgh)

  • De-dong Li

    (University of Pittsburgh
    University of Pittsburgh)

  • Shuxia Wang

    (University of Pittsburgh)

  • Godhev K. Manakkat Vijay

    (University of Pittsburgh
    University of Pittsburgh)

  • Isha Mehta

    (University of Pittsburgh
    University of Pittsburgh)

  • Raymond West

    (University of Pittsburgh)

  • Muthusamy Thangaraju

    (Augusta University)

  • Thomas D. Nolin

    (University of Pittsburgh)

  • Jishnu Das

    (University of Pittsburgh
    University of Pittsburgh)

  • John F. Alcorn

    (University of Pittsburgh
    University of Pittsburgh)

  • Partha S. Biswas

    (University of Pittsburgh
    University of Pittsburgh
    Stony Brook University)

Abstract

Antibody-mediated protection against pathogens is crucial to a healthy life. However, the recent SARS-CoV-2 pandemic has shown that pre-existing comorbid conditions including kidney disease account for compromised humoral immunity to infections. Individuals with kidney disease are not only susceptible to infections but also exhibit poor vaccine-induced antibody response. Using multiple mouse models of kidney disease, we demonstrate that renal dysfunction inhibits germinal center (GC) response against T-dependent antigens. GC B cells exhibit increased apoptosis in kidney disease. Uremic toxin hippuric acid drives loss of mitochondrial membrane potential, leading to increased apoptosis of GC B cells in a G-protein–coupled receptor 109A dependent manner. Finally, GC B cells and antibody titer are diminished in mice with kidney disease following influenza virus infection, a major cause of mortality in individuals with renal disorders. These results provide a mechanistic understanding of how renal dysfunction suppresses humoral immunity in patients with kidney disease.

Suggested Citation

  • Doureradjou Peroumal & Chetan V. Jawale & Wonseok Choi & Hossein Rahimi & Danielle Antos & De-dong Li & Shuxia Wang & Godhev K. Manakkat Vijay & Isha Mehta & Raymond West & Muthusamy Thangaraju & Thom, 2024. "The survival of B cells is compromised in kidney disease," Nature Communications, Nature, vol. 15(1), pages 1-19, December.
  • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-55187-w
    DOI: 10.1038/s41467-024-55187-w
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    References listed on IDEAS

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    1. Takuya Nojima & Kei Haniuda & Tatsuya Moutai & Moeko Matsudaira & Sho Mizokawa & Ikuo Shiratori & Takachika Azuma & Daisuke Kitamura, 2011. "In-vitro derived germinal centre B cells differentially generate memory B or plasma cells in vivo," Nature Communications, Nature, vol. 2(1), pages 1-11, September.
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