Journal
TOXINS
Volume 9, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/toxins9100293
Keywords
immune response; intracellular pathways; phagocytosis; T-helper cells
Categories
Funding
- EATRIS-CZ project - Operational Programme Research, Development and Education [CZ.02.1.01/0.0/0.0/16_013/0001818]
- Charles University, project GA UK [507116]
- [NV16-28126A]
- [GA13-145475]
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Adenylate cyclase toxin (CyaA) is released in the course of B. pertussis infection in the host's respiratory tract in order to suppress its early innate and subsequent adaptive immune defense. CD11b-expressing dendritic cells (DC), macrophages and neutrophils are professional phagocytes and key players of the innate immune system that provide a first line of defense against invading pathogens. Recent findings revealed the capacity of B. pertussis CyaA to intoxicate DC with high concentrations of 3,5-cyclic adenosine monophosphate (cAMP), which ultimately skews the host immune response towards the expansion of Th17 cells and regulatory T cells. CyaA-induced cAMP signaling swiftly incapacitates opsonophagocytosis, oxidative burst and NO-mediated killing of bacteria by neutrophils and macrophages. The subversion of host immune responses by CyaA after delivery into DC, macrophages and neutrophils is the subject of this review.
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