Abstract
Infection with Neisseria gonorrhoeae can trigger an intense inflammatory response, yet there is little specific immune response or development of immune memory. In addition, gonorrhea typically correlates with a transient reduction in T lymphocyte counts in blood, and these populations recover when gonococcal infection is resolved. Such observations suggest that the gonococci have a suppressive effect on the host immune response. We report here that N. gonorrhoeae Opa proteins were able to bind CEACAM1 expressed by primary CD4+ T lymphocytes and suppress their activation and proliferation. CEACAM1 bound by gonococcal Opa52 associated with the tyrosine phosphatases SHP-1 and SHP-2, which implicates the receptor's ITIM (immunoreceptor tyrosine-based inhibitory motif) in this effect.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antigens, CD / analysis
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Antigens, CD / physiology*
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Antigens, Differentiation / analysis
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Antigens, Differentiation / physiology*
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Antigens, Differentiation, T-Lymphocyte / physiology
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CD4-Positive T-Lymphocytes / immunology*
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Cell Adhesion Molecules
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Cell Death
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Gonorrhea / immunology*
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Humans
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Immune Tolerance*
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Intracellular Signaling Peptides and Proteins
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Lectins, C-Type
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Lymphocyte Activation*
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Protein Tyrosine Phosphatase, Non-Receptor Type 11
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Protein Tyrosine Phosphatase, Non-Receptor Type 6
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Protein Tyrosine Phosphatases / physiology
Substances
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Antigens, CD
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Antigens, Differentiation
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Antigens, Differentiation, T-Lymphocyte
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CD66 antigens
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CD69 antigen
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Cell Adhesion Molecules
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Intracellular Signaling Peptides and Proteins
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Lectins, C-Type
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PTPN11 protein, human
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PTPN6 protein, human
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Protein Tyrosine Phosphatase, Non-Receptor Type 11
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Protein Tyrosine Phosphatase, Non-Receptor Type 6
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Protein Tyrosine Phosphatases