Molecular Mechanism behind Monocyte Phagocytosis-Induced Cell Death
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".
Deadline for manuscript submissions: 20 January 2025 | Viewed by 202
Special Issue Editor
Interests: sepsis; immunology of infectious diseases; innate immunity; inflammation; infection; macrophage; macrophage biology; monocyte-macrophage; phagocytosis; immunology of premature and newborn babies
Special Issue Information
Dear Colleagues,
The ability to detect pathogen-associated molecular patterns (PAMPs) via pattern recognition receptors (PRRs) is the initial point of phagocytosis and phagocytosis-induced cell death (PICD). The binding, phagocytosis and intracellular degradation in the phagolysosome are subsequent steps leading to pathogen clearance, which is one of the main monocyte functions.
Dysregulation or imbalance of PICD in the host is accompanied by a variety of pathophysiological consequences. If monocytes undergo abortive PICD, bacteria may survive which could cause latent infection. In the case of delayed or insufficient PICD, permanent or prolonged cytokine production via activated effector cells causes sustained inflammation and systemic damage to the host. Effector cell apoptosis is therefore tightly regulated.
Numerous apoptotic signaling pathways rely on a balance of pro- and anti-apoptotic factors. In comparison to PBMC, CBMC expresses a higher level of anti-apoptotic proteins such as B-Cell lymphoma 2 (Bcl-2) family, whereas the expression of pro-apoptotic proteins is diminished. A higher expression of Bcl-2 and Bcl-XL downregulates cleaved Caspase-3 and Caspase-9 and the intrinsic apoptotic pathway. On the other hand, the extrinsic apoptotic pathway is enabled by CD95L/CD95 and TNF-α/TNFR1 pairs of death ligand/death receptors. It is found reduced in neonatal monocytes. Non-phagocytosing, TNF-α presenting and secreting monocytes kill their mates, which do not contribute to combatting pathogens via an autocrine and paracrine mechanism. This phenomenon called “bystander kill” or “fratricide” is also reduced in CBMC.
These exemplary findings illustrate the variety of factors which are engaged in PICD. The present special issue is intended to shed light to this complex phenomenon contributing to host defense reactions.
Dr. Stephan Dreschers
Guest Editor
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Keywords
- monocyte phagocytosis
- phagocytosis-induced cell death
- pattern recognition receptors
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