About this Research Topic
Myeloid cells such as dendritic cells (DCs) have a crucial role in the initiation of immune responses. As professional antigen-presenting cells, they are not only involved in the recognition and ingestion of pathogens but also in the subsequent presentation of antigens to T cells. Thereby, tailored immune responses against the pathogen are mounted. However, pathogens use different mechanisms to evade immune responses.
Several pathogens, such as viruses (e.g. Influenza, SARS-CoV-2) and bacteria (e.g. B. anthracis, M. tuberculosis) express molecules that activate the inflammasome in the host cell. Activation of the inflammasome typically induces pyroptosis, an inflammatory form of cell death. As cell death is detrimental to the subsequent induction of T-cell responses, activation of cell death in antigen-presenting cells might represent an evasion strategy for different pathogens. However, certain antigen-presenting cells, such as monocytes and dendritic cells, seem to be able to avoid pyroptosis and enter a state of hyperactivation in response to the activation of inflammasomes or suppress the activation of inflammasomes. Thereby, the cells might preserve their capacity to induce immune responses against the pathogen.
In addition to infection, danger-associated molecular patterns (DAMPs) are released from necrotic cells in the absence of any pathogens during sterile inflammation. Here, DAMPs, such as ATP and HMGB1, might activate the NLRP3 inflammasome leading to release of the proinflammatory cytokine IL-1β as well as pyroptosis or hyperactivation in the responding cell. Sterile inflammation is involved in several chronic inflammatory diseases, such as gout, Atherosclerosis and Alzheimer’s disease, but also in cancer. How recognition of DAMPs by APCs during sterile inflammation influences their function and whether induction of pyroptosis limits further inflammation by APCs, is not clear, yet.
Thus, the focus of this special issue will be on the influence of cell death pathways on the function of APCs and the role of cell death during the interaction of pathogens and immune cells as potential evasion strategy. This might not only be limited to pyroptosis but also to other cell death pathways, such as apoptosis, necrosis, necroptosis, and ferroptosis. Specific topics might include:
• Identification of specific pathways in how pathogens induce cell death in antigen-presenting cells
• How do antigen-presenting cells prevent undergoing cell death in response to certain pathogens?
• Does inhibition of certain cell death pathways in antigen-presenting cells improve the immune response to pathogens?
• How does the type of cell death of infected host cells influence the capacity of antigen-presenting cells to induce immune responses?
• Does the cell death pathway induced by a pathogen shape the subsequent immune response?
• How react APCs to DAMPs released by necrotic cells during sterile inflammation?
• Which receptors and signaling pathways in APCs are involved in the recognition of different forms of cell death?
Several pathogens, such as viruses (e.g. Influenza, SARS-CoV-2) and bacteria (e.g. B. anthracis, M. tuberculosis) express molecules that activate the inflammasome in the host cell. Activation of the inflammasome typically induces pyroptosis, an inflammatory form of cell death. As cell death is detrimental to the subsequent induction of T-cell responses, activation of cell death in antigen-presenting cells might represent an evasion strategy for different pathogens. However, certain antigen-presenting cells, such as monocytes and dendritic cells, seem to be able to avoid pyroptosis and enter a state of hyperactivation in response to the activation of inflammasomes or suppress the activation of inflammasomes. Thereby, the cells might preserve their capacity to induce immune responses against the pathogen.
In addition to infection, danger-associated molecular patterns (DAMPs) are released from necrotic cells in the absence of any pathogens during sterile inflammation. Here, DAMPs, such as ATP and HMGB1, might activate the NLRP3 inflammasome leading to release of the proinflammatory cytokine IL-1β as well as pyroptosis or hyperactivation in the responding cell. Sterile inflammation is involved in several chronic inflammatory diseases, such as gout, Atherosclerosis and Alzheimer’s disease, but also in cancer. How recognition of DAMPs by APCs during sterile inflammation influences their function and whether induction of pyroptosis limits further inflammation by APCs, is not clear, yet.
Thus, the focus of this special issue will be on the influence of cell death pathways on the function of APCs and the role of cell death during the interaction of pathogens and immune cells as potential evasion strategy. This might not only be limited to pyroptosis but also to other cell death pathways, such as apoptosis, necrosis, necroptosis, and ferroptosis. Specific topics might include:
• Identification of specific pathways in how pathogens induce cell death in antigen-presenting cells
• How do antigen-presenting cells prevent undergoing cell death in response to certain pathogens?
• Does inhibition of certain cell death pathways in antigen-presenting cells improve the immune response to pathogens?
• How does the type of cell death of infected host cells influence the capacity of antigen-presenting cells to induce immune responses?
• Does the cell death pathway induced by a pathogen shape the subsequent immune response?
• How react APCs to DAMPs released by necrotic cells during sterile inflammation?
• Which receptors and signaling pathways in APCs are involved in the recognition of different forms of cell death?
Keywords: cell death, dendritic cells, antigen-presenting cells, inflammasome, pyroptosis, DAMPs
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