Neisseria gonorrhoeae Kills Carcinoembryonic Antigen-Related Cellular Adhesion Molecule 1 (CD66a)-Expressing Human B Cells and Inhibits Antibody Production Export

@article{citeulike:3171014, abstract = {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 OpaI 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. 10.1128/IAI.73.7.4171-4179.2005}, author = {Pantelic, Milica and Kim, Young-June and Bolland, Silvia and Chen, Ines and Shively, John and Chen, Tie}, citeulike-article-id = {3171014}, citeulike-linkout-0 = {http://dx.doi.org/10.1128/IAI.73.7.4171-4179.2005}, citeulike-linkout-1 = {http://iai.asm.org/cgi/content/abstract/73/7/4171}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/15972507}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=15972507}, day = {1}, doi = {10.1128/IAI.73.7.4171-4179.2005}, journal = {Infect. Immun.}, keywords = {ceacam, gonorrhoeae, opai}, month = {July}, number = {7}, pages = {4171--4179}, posted-at = {2008-08-29 04:04:25}, priority = {3}, title = {Neisseria gonorrhoeae Kills Carcinoembryonic Antigen-Related Cellular Adhesion Molecule 1 (CD66a)-Expressing Human B Cells and Inhibits Antibody Production}, url = {http://dx.doi.org/10.1128/IAI.73.7.4171-4179.2005}, volume = {73}, year = {2005} }

TY - JOUR ID - citeulike:3171014 L3 - citeulike-article-id:3171014 N2 - 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 OpaI 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. 10.1128/IAI.73.7.4171-4179.2005 IS - 7 JF - Infect. Immun. EP - 4179 TI - Neisseria gonorrhoeae Kills Carcinoembryonic Antigen-Related Cellular Adhesion Molecule 1 (CD66a)-Expressing Human B Cells and Inhibits Antibody Production VL - 73 SP - 4171 KW - ceacam KW - gonorrhoeae KW - opai AU - Pantelic, Milica AU - Kim, Young-June AU - Bolland, Silvia AU - Chen, Ines AU - Shively, John AU - Chen, Tie PY - 2005/07/01/ UR - http://dx.doi.org/10.1128/IAI.73.7.4171-4179.2005 ER -