Staphylococcal Protein A Deletes B-1a and Marginal Zone B Lymphocytes Expressing Human Immunoglobulins: An Immune Evasion Mechanism

Protein A (SpA) of Staphylococcus aureus is endowed with the capacity to interact with the H chain variable region (V(H)) of human Abs and to target >40% of B lymphocytes. To investigate whether this property represents a virulence factor and to determine the in vivo consequences of the confronta...

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Bibliographic Details
Published in:Journal of Immunology 2005-12, Vol.175 (11), p.7719-7727
Main Authors: Viau, Muriel, Longo, Nancy S, Lipsky, Peter E, Zouali, Moncef
Format: Article
Language:English
Subjects:
Animals
B-Lymphocyte Subsets - immunology
B-Lymphocytes - immunology
Enzyme-Linked Immunosorbent Assay
Flow Cytometry
Fluorescent Antibody Technique
Humans
Immunoglobulin Variable Region - genetics
Immunoglobulin Variable Region - immunology
Mice
Mice, Transgenic
Peritoneal Cavity - cytology
Polymerase Chain Reaction
Recombinant Proteins - immunology
Spleen - cytology
Spleen - immunology
Staphylococcal Protein A - immunology
Staphylococcus aureus
Staphylococcus aureus - immunology
Staphylococcus aureus - pathogenicity
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Summary:Protein A (SpA) of Staphylococcus aureus is endowed with the capacity to interact with the H chain variable region (V(H)) of human Abs and to target >40% of B lymphocytes. To investigate whether this property represents a virulence factor and to determine the in vivo consequences of the confrontation of SpA with B lymphocytes, we used transgenic mice expressing fully human Abs. We found that administration of soluble SpA reduces B-1a lymphocytes of the peritoneal cavity and marginal zone B lymphocytes of the spleen, resulting in a markedly deficient type 2 humoral response. Single-cell PCR analysis and sequencing of the Ab V(H) gene repertoire revealed a significant reduction of V(H)3+ marginal zone B cells. Since the two B lymphocyte subsets targeted are involved in innate immune functions, our data suggest that crippling of humoral immunity by S. aureus represents an immune evasion mechanism that may aggravate recurrent infections.
ISSN:0022-1767
1550-6606
1365-2567
DOI:10.4049/jimmunol.175.11.7719