Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 211, Issue 12, Pages 2331-2339Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20141404
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Funding
- National Institutes of Health [1U19AI08724, 5U54AI057158, 5U19AI057266, 1U19AI090023, 1P01AI097092, 1RC4AI092711-01]
- American Heart Association [13PRE16420013]
- National Institute of Allergy and Infectious Disease Interdisciplinary Training Program in Immunology [T32AI007090]
- Gwen Knapp Center for Lupus and Immunology Research
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Staphylococcus aureus bacterial infection commonly results in chronic or recurrent disease, suggesting that humoral memory responses are hampered. Understanding how S. aureus subverts the immune response is critical for the rescue of host natural humoral immunity and vaccine development. S. aureus expresses the virulence factor Protein A (SpA) on all clinical isolates, and SpA has been shown in mice to expand and ablate variable heavy 3 (VH3) idiotype B cells. The effects of SpA during natural infection, however, have not been addressed. Acutely activated B cells, or plasmablasts (PBs), were analyzed to dissect the ongoing immune response to infection through the production of monoclonal antibodies (mAbs). The B cells that were activated by infection had a highly limited response. When screened against multiple S. aureus antigens, only high-affinity binding to SpA was observed. Consistently, PBs underwent affinity maturation, but their B cell receptors demonstrated significant bias toward the VH3 idiotype. These data suggest that the superantigenic activity of SpA leads to immunodominance, limiting host responses to other S. aureus virulence factors that would be necessary for protection and memory formation.
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