Table 1.

Neisseria gonorrhoeae Manipulates Host Immunity for its Own Advantage

Activity	Reference
Opa proteins interact with CEACAM1 and inactivate CD4+ T cells	[17]
Opa proteins interact with CEACAM3 on neutrophils	[18]
N. gonorrhoeae inhibits intracellular killing mechanisms in neutrophils	[19]
N. gonorrhoeae inhibits killing by antimicrobial peptides using MtrCDE efflux pump	[20]
PorB inhibits DC-induced CD4+ T-cell proliferation	[21]
Gonococcal infection induces Th17-driven innate immune responses	[22, 23]
N. gonorrhoeae suppresses Th1/Th2-driven adaptive immune responses by inducing TGF-β, IL-10, and type 1 regulatory T cells	[24, 25]
N. gonorrhoeae modulates macrophage differentiation into “alternative” M2 pathway	[26]
N. gonorrhoeae induces NLRP3-dependent pyronecrosis of monocytes	[27]

Abbreviations: CEACAM, carcinoembryonic antigen-related cell adhesion molecule; DC, dendritic cell; IL-10, interleukin-10; Opa, opacity; PorB, porin; TGF-β, transforming growth factor-β; Th, T helper.