Dendritic Cells in Health and Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (15 February 2024) | Viewed by 3315

Special Issue Editor


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Guest Editor
Pathology & Immunology, Baylor College of Medicine, Houston, TX, USA
Interests: cancer vaccination; dendritic cell immunobiology; TH polarization; immune cell signaling; non-lymphoid CTLA-4

Special Issue Information

Dear Colleagues,

As the principal cell types through which environmental cues and danger signals are detected, integrated, and transmitted to immune effectors, dendritic cells occupy a dominant position atop the hierarchy of the adaptive immune system. Whether adaptive immunity triumphs or errs, the ultimate consequence is substantially dependent upon the manner in which dendritic cells interpret the myriad of signals that inform immune outcomes as well as specific polymorphisms and mutations that shape their function and phenotype. Thus, any study providing insight into these critical topics will be of interest to this Special Issue, particularly if the results provide novel insights into dendritic cell governance of immune homeostasis in health and disease.

Dr. William K. Decker
Guest Editor

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Keywords

  • immune homeostasis
  • TH polarization
  • signaling
  • interferon
  • central tolerance
  • peripheral tolerance
  • exosomes
  • microRNAs
  • cytokines
  • chemokines

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Published Papers (2 papers)

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Research

15 pages, 2828 KiB  
Article
Reduced Tolerogenic Program Death-Ligand 1-Expressing Conventional Type 1 Dendritic Cells Are Associated with Rapid Decline in Chronic Obstructive Pulmonary Disease
by Kuan-Yuan Chen, Wei-Lun Sun, Sheng-Ming Wu, Po-Hao Feng, Chiou-Feng Lin, Tzu-Tao Chen, Yueh-Hsun Lu, Shu-Chuan Ho, Yueh-Hsi Chen and Kang-Yun Lee
Cells 2024, 13(10), 878; https://doi.org/10.3390/cells13100878 - 20 May 2024
Cited by 1 | Viewed by 1194
Abstract
Background: Chronic obstructive pulmonary disease (COPD) is characterized, at least in part, by autoimmunity through amplified T helper 1 and 17 (Th1 and Th17) immune responses. The loss of immune tolerance controlled by programmed death-ligand 1 (PD-L1) may contribute to this. Objectives: We [...] Read more.
Background: Chronic obstructive pulmonary disease (COPD) is characterized, at least in part, by autoimmunity through amplified T helper 1 and 17 (Th1 and Th17) immune responses. The loss of immune tolerance controlled by programmed death-ligand 1 (PD-L1) may contribute to this. Objectives: We studied the tolerogenic role of PD-L1+ dendritic cells (DCs) and their subtypes in relation to specific T cell immunity and the clinical phenotypes of COPD. Methods: We used flow cytometry to analyze PD-L1 expression by the DCs and their subtypes in the peripheral blood mononuclear cells (PBMCs) from normal participants and those with COPD. T cell proliferation and the signature cytokines of T cell subtypes stimulated with elastin as autoantigens were measured using flow cytometry and enzyme-linked immunosorbent assays (ELISA), respectively. Measurement and main results: A total of 83 participants were enrolled (normal, n = 29; COPD, n = 54). A reduced PD-L1+ conventional dendritic cell 1 (cDC1) ratio in the PBMCs of the patients with COPD was shown (13.7 ± 13.7%, p = 0.03). The decrease in the PD-L1+ cDC1 ratio was associated with a rapid decline in COPD (p = 0.02) and correlated with the CD4+ T cells (r = −0.33, p = 0.02). This is supported by the NCBI GEO database accession number GSE56766, the researchers of which found that the gene expressions of PD-L1 and CD4, but not CD8 were negatively correlated from PBMC in COPD patients (r = −0.43, p = 0.002). Functionally, the PD-L1 blockade enhanced CD4+ T cell proliferation stimulated by CD3/elastin (31.2 ± 22.3%, p = 0.04) and interleukin (IL)-17A production stimulated by both CD3 (156.3 ± 54.7, p = 0.03) and CD3/elastin (148 ± 64.9, p = 0.03) from the normal PBMCs. The PD-L1 blockade failed to increase IL-17A production in the cDC1-depleted PBMCs. By contrast, there was no significant change in interferon (IFN)-γ, IL-4, or IL-10 after the PD-L1 blockade. Again, these findings were supported by the NCBI GEO database accession number GSE56766, the researchers of which found that only the expression of RORC, a master transcription factor driving the Th17 cells, was significantly negatively correlated to PD-L1 (r = −0.33, p = 0.02). Conclusions: Circulating PD-L1+ cDC1 was reduced in the patients with COPD, and the tolerogenic role was suppressed with susceptibility to self-antigens and linked to rapid decline caused by Th17-skewed chronic inflammation. Full article
(This article belongs to the Special Issue Dendritic Cells in Health and Disease)
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24 pages, 5762 KiB  
Article
Exploiting Leishmania—Primed Dendritic Cells as Potential Immunomodulators of Canine Immune Response
by Ana Valério-Bolas, Mafalda Meunier, Joana Palma-Marques, Armanda Rodrigues, Ana Margarida Santos, Telmo Nunes, Rui Ferreira, Ana Armada, João Carlos Alves, Wilson Antunes, Inês Cardoso, Sofia Mesquita-Gabriel, Lis Lobo, Graça Alexandre-Pires, Luís Marques, Isabel Pereira da Fonseca and Gabriela Santos-Gomes
Cells 2024, 13(5), 445; https://doi.org/10.3390/cells13050445 - 3 Mar 2024
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Abstract
Dendritic cells (DCs) capture pathogens and process antigens, playing a crucial role in activating naïve T cells, bridging the gap between innate and acquired immunity. However, little is known about DC activation when facing Leishmania parasites. Thus, this study investigates in vitro activity [...] Read more.
Dendritic cells (DCs) capture pathogens and process antigens, playing a crucial role in activating naïve T cells, bridging the gap between innate and acquired immunity. However, little is known about DC activation when facing Leishmania parasites. Thus, this study investigates in vitro activity of canine peripheral blood-derived DCs (moDCs) exposed to L. infantum and L. amazonensis parasites and their extracellular vesicles (EVs). L. infantum increased toll-like receptor 4 gene expression in synergy with nuclear factor κB activation and the generation of pro-inflammatory cytokines. This parasite also induced the expression of class II molecules of major histocompatibility complex (MHC) and upregulated co-stimulatory molecule CD86, which, together with the release of chemokine CXCL16, can attract and help in T lymphocyte activation. In contrast, L. amazonensis induced moDCs to generate a mix of pro- and anti-inflammatory cytokines, indicating that this parasite can establish a different immune relationship with DCs. EVs promoted moDCs to express class I MHC associated with the upregulation of co-stimulatory molecules and the release of CXCL16, suggesting that EVs can modulate moDCs to attract cytotoxic CD8+ T cells. Thus, these parasites and their EVs can shape DC activation. A detailed understanding of DC activation may open new avenues for the development of advanced leishmaniasis control strategies. Full article
(This article belongs to the Special Issue Dendritic Cells in Health and Disease)
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