The Journal of Infectious Diseases · 1997 · 37 citations · 51 references
Life SciencesImmunologyMicrobiologyImmunology Of Infectious DiseasesImmunoregulationInnate ImmunityCell-mediated ImmunityCellular Immune ResponsesCellular Immunity In InfectionComplement SystemMacrophage BiologyPhagocyte BiologyAdenylate Cyclase SignalingComplement In Host DefenseComplement In ImmunityComplement In Infectious DiseaseExogenous Antigen PresentationImmune Cell Proliferation InhibitionLymphocyte Proliferation InhibitionMonocyte Biology
Human monocytes and macrophages bind Bordetella pertussis through multiple specific receptor-ligand interactions; however, the effect of these interactions on monocyte and macrophage function is not well understood. In an in vitro system, B. pertussis infection of human monocytes significantly impaired T cell proliferation to exogenous antigen at MOIs as low as 1.0. B. pertussis isogenic mutant strains deficient in filamentous hemagglutinin or adenylate cyclase toxin were incapable of proliferation inhibition, suggesting that these virulence-associated factors are essential for this activity. B. pertussis-induced monocyte death alone did not explain these results, nor did differences in intracellular survival. In addition, B. pertussis infection did not significantly alter monocyte phagocytosis of complement-opsonized latex particles, indicating that B. pertussis infection does not globally impair monocyte functions in this system. These results suggest that B. pertussis may be capable of subverting cellular immune defenses in an infected host.
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Inhibition by cAMP of Ras-Dependent Activation of Raf
Simon J. Cook, Frank McCormick · Science · 1993 · 940 citations
Tn5-induced mutations affecting virulence factors of Bordetella pertussis
Alison A. Weiss, Erik L. Hewlett, G A Myers et al. · Infection and Immunity · 1983 · 396 citations · Full text