Gonococcal immune suppression

Patients infected with Neisseria gonorrhoea present with intense inflammation resulting in urethral or cervical pus discharge, but the specific immune response to the bacteria is weak and does not protect against subsequent gonococcal infections. In February 19 online Nature Immunology, Ian Boulton and Scott Gray-Owen from University of Toronto, Canada, show that N. gonorrhoea have a mechanism that can arrest the activation and proliferation of CD4+ T lymphocytes via the CEACAM1 adhesion molecul

Tudor Toma(t.toma@ic.ac.uk)
Feb 17, 2002

Patients infected with Neisseria gonorrhoea present with intense inflammation resulting in urethral or cervical pus discharge, but the specific immune response to the bacteria is weak and does not protect against subsequent gonococcal infections. In February 19 online Nature Immunology, Ian Boulton and Scott Gray-Owen from University of Toronto, Canada, show that N. gonorrhoea have a mechanism that can arrest the activation and proliferation of CD4+ T lymphocytes via the CEACAM1 adhesion molecules.

Boulton and Gray-Owen observed that gonococci expressing colony opacity-associated (Opa) proteins bound CEACAM1 receptors and inhibited the activation and proliferation of primary human CD4+ T lymphocytes in response to otherwise activating stimuli. Isogenic strains of N. gonorrhoea expressing adhesins that did not bind to CEACAM1 did not induce comparable inhibition. In addition, they showed that a CEACAM-specific antibody mimicked the bacterial suppression of the T lymphocyte response (Nat Immunol 2002, DOI: 10.1038/ni769)....

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