Activated Apoptotic Cells Induce Dendritic Cell Maturation via Engagement of Toll-like Receptor 4 (TLR4), Dendritic Cell-specific Intercellular Adhesion Molecule 3 (ICAM-3)-grabbing Nonintegrin (DC-SIGN), and β2 Integrins

Abstract

Background: Activated apoptotic lymphocytes provide activation/maturation signals to human monocyte-derived dendritic cells (DCs). Results: Cell-cell contact-dependent signaling involved ␤2 integrins, DC-SIGN, and TLR4, which resulted in activation of multiple signaling pathways. Conclusion: These studies provide mechanistic insight into DC responses during encounter with cells undergoing immunogenic cell death. Significance: Learning how DCs respond to certain cell death has implications for vaccine design.

Effects of porcine epidemic diarrhea virus on porcine monocyte-derived dendritic cells and intestinal dendritic cells

“…central role in initiating the adaptive immune response against infecting agents. DC maturation is accompanied by the regulation of major histocompatibility complex class I (MHC-I) and class II (MHC-II, designated SLA-II-DR in swine) proteins, co-stimulatory factors (CD80/86), as well as factors involved in cell adhesion (Kruse et al, 2000;Pathak et al, 2012). IL-12 is secreted by mature DCs to facilitate the effective priming of type 1 cytokine-producing T cells to resist viral infection (Anthony et al, 2004).…”

Consensus guidelines for the detection of immunogenic cell death

“…This said, extracellular HMGB1 is well known to mediate robust proinflammatory effects upon binding to several receptors on the surface of immune cells, including TLR2, TLR4 and advanced glycosylation end product-specific receptor (AGER, best known as RAGE). [202][203][204][205][206][207][208][209][210] Moreover, extracellular HMGB1 reportedly exerts a chemotactic activity by forming a complex with chemokine (C-X-C motif) ligand 12 (CXCL12) that signals via chemokine (C-X-C motif) receptor 4 (CXCR4). 211 Finally, at least under some circumstances, endogenous HMGB1 appears to promote autophagy by interfering with the mutually inhibitory interaction between the central autophagic regulator beclin 1 (BECN1) and the anti-apoptotic protein B-cell CLL/lymphoma 2 (BCL2).…”

Systemic Clearance of Radiation-Induced Apoptotic Cells by SIGN-R1 and Complement Factors and their Involvement in Autoimmune Diseases

“…Autoimmune diseases are a serious public health problems [33] and there is increasing evidence that C-type lectins and complement system are involved in the pathogenesis of the autoimmune diseases [34][35][36][37][38]. We introduced the new systemic clearance mechanism of radiation-induced apoptotic cells, in which SIGN-R1 could initiate and enhance the clearance of apoptotic cells by activating the complement deposition pathway against apoptotic cells in the spleen, integrating the role of SIGN-R1 and complements in the clearance of radiationinduced apoptotic cells.…”