Journal
INFECTION AND IMMUNITY
Volume 73, Issue 7, Pages 4171-4179Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.73.7.4171-4179.2005
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Funding
- FIC NIH HHS [R03TW006270, R03 TW006270] Funding Source: Medline
- NIAID NIH HHS [R01 AI047736] Funding Source: Medline
- PHS HHS [R01A1 47736] Funding Source: Medline
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Neisseria gonorrhoeae cells (gonococci [GC]), the etiological agents for gonorrhea, can cause repeated infections. During and after gonococcal infection, local and systemic antigonococcal antibody levels are low. These clinical data indicate the possibility that GC may suppress immune responses during infection. Carcinoembryonic antigen-related cellular adhesion molecule 1 (CEACAM1 or CD66a), a receptor for GC opacity (Opa) proteins, was shown to mediate inhibitory signals. In the present study, human B cells were activated by interleukin-2 to express CEACAM1 and then stimulated to secrete antibodies and simultaneously coincubated with Opa(-) and Opal GC of strain MS11. Our results show that this OpaI GC has the ability to inhibit antibody production. The interaction of GC and CEACAM1 with human peripheral B cells also results in induction of cell death. The same findings were observed in DT40 B cells. This CEACAM1-promoted cell death pathway does not involve the inhibitory signals or the tyrosine phosphatases SHP-1 and SHP-2 but depends on Bruton's tyrosine kinase in DT40 cells. Our results suggest that Neisseria gonorrhoeae possesses the ability to suppress antibody production by killing CEACAM1-expressing B cells.
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