Dendritic cells (DCs) play a central role in the immune response by presenting antigens to naïve T cells and therefore, triggering the adaptive arm of the immune response.
The actions against the invading pathogens are either direct (e.g. phagocytosis and killing) or indirect through the release of cytokines or other stimulatory molecules, which trigger the adaptive immune system by activating B cells and T cells.
Actions against the invading pathogens are either direct (e.g. phagocytosis and killing) or indirect, through release of cytokines or other stimulatory molecules that trigger the adaptive immune system by activating B and T cells.
The challenges imposed by changing environmental conditions, such as those often associated with speciation and species range expansions, might thus trigger the adaptive evolution of ORs and also promote adaptive regulatory changes in the chemoreceptor genes.
Thus, the initial increase in DC formation after necrosis of infected macrophages is caused by the increase in the number of extracellular bacilli, therefore a sudden increase in DCs could potentially trigger the adaptive immunity.
This presentation in turn triggers the adaptive immune response against the antigen.
Autophagy is triggered primarily by the adaptive response action of the chief transcriptional regulator HIF-1 α, which in addition to activating a large cassette of target genes activates the transcription of Bnip3 and Bnip3L, both essential for hypoxia-induced autophagy.
Preclinical experiments suggest that AS03 enhances the adaptive responses to vaccine antigens by triggering a transient innate response local to the injection site [ 23].
However, the discovery that microbial products activate host cells via pattern recognition receptors such as Toll-like receptors (TLRs) and enhance adaptive immune responses by triggering cytokine production and dendritic cell maturation, has led to TLR agonists being developed as vaccine adjuvants [14] [18].
This in turn is suggested to trigger the innate and adaptive immune response.
