scholarly journals Regulation of Hemichannels and Gap Junction Channels by Cytokines in Antigen-Presenting Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-23 ◽  
Author(s):  
Pablo J. Sáez ◽  
Kenji F. Shoji ◽  
Adam Aguirre ◽  
Juan C. Sáez
Keyword(s):  
Immune System ◽  
Gap Junction ◽  
Immune Cells ◽  
Intercellular Communication ◽  
Purinergic Signaling ◽  
Antigen Presenting Cells ◽  
Cell Types ◽  
Gap Junction Channels ◽  
Extracellular Milieu ◽  
Antigen Presenting

Autocrine and paracrine signals coordinate responses of several cell types of the immune system that provide efficient protection against different challenges. Antigen-presenting cells (APCs) coordinate activation of this system via homocellular and heterocellular interactions. Cytokines constitute chemical intercellular signals among immune cells and might promote pro- or anti-inflammatory effects. During the last two decades, two membrane pathways for intercellular communication have been demonstrated in cells of the immune system. They are called hemichannels (HCs) and gap junction channels (GJCs) and provide new insights into the mechanisms of the orchestrated response of immune cells. GJCs and HCs are permeable to ions and small molecules, including signaling molecules. The direct intercellular transfer between contacting cells can be mediated by GJCs, whereas the release to or uptake from the extracellular milieu can be mediated by HCs. GJCs and HCs can be constituted by two protein families: connexins (Cxs) or pannexins (Panxs), which are present in almost all APCs, being Cx43 and Panx1 the most ubiquitous members of each protein family. In this review, we focus on the effects of different cytokines on the intercellular communication mediated by HCs and GJCs in APCs and their impact on purinergic signaling.

scholarly journals Neuroinflammation in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia and the Interest of Induced Pluripotent Stem Cells to Study Immune Cells Interactions With Neurons

2021 ◽  
Vol 14 ◽  
Author(s):  
Elise Liu ◽  
Léa Karpf ◽  
Delphine Bohl
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Immune System ◽  
Frontotemporal Dementia ◽  
Immune Cells ◽  
Immune Cell ◽  
Current Knowledge ◽  
Cell Types ◽  
Induced Pluripotent ◽  
Different Cell Types ◽  
Lateral Sclerosis

Inflammation is a shared hallmark between amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). For long, studies were conducted on tissues of post-mortem patients and neuroinflammation was thought to be only bystander result of the disease with the immune system reacting to dying neurons. In the last two decades, thanks to improving technologies, the identification of causal genes and the development of new tools and models, the involvement of inflammation has emerged as a potential driver of the diseases and evolved as a new area of intense research. In this review, we present the current knowledge about neuroinflammation in ALS, ALS-FTD, and FTD patients and animal models and we discuss reasons of failures linked to therapeutic trials with immunomodulator drugs. Then we present the induced pluripotent stem cell (iPSC) technology and its interest as a new tool to have a better immunopathological comprehension of both diseases in a human context. The iPSC technology giving the unique opportunity to study cells across differentiation and maturation times, brings the hope to shed light on the different mechanisms linking neurodegeneration and activation of the immune system. Protocols available to differentiate iPSC into different immune cell types are presented. Finally, we discuss the interest in studying monocultures of iPS-derived immune cells, co-cultures with neurons and 3D cultures with different cell types, as more integrated cellular approaches. The hope is that the future work with human iPS-derived cells helps not only to identify disease-specific defects in the different cell types but also to decipher the synergistic effects between neurons and immune cells. These new cellular tools could help to find new therapeutic approaches for all patients with ALS, ALS-FTD, and FTD.

Infection and immunity

2021 ◽  
pp. 853-920
Keyword(s):  
Major Histocompatibility Complex ◽  
Immune System ◽  
Cell Types ◽  
The Body ◽  
Acquired Immunity ◽  
Histocompatibility Complex ◽  
Repair Mechanisms ◽  
Antigen Presenting ◽  
Different Cell Types

‘Infection and immunity’ considers the response of the body to pathogens, such as bacteria, viruses, prions, fungi, and parasites, which are discussed in terms of their nature, life cycle, and modes of infection. The role of the immune system in defence against infection is discussed, including innate and adaptive (acquired) immunity, antigens, the major histocompatibility complex, and the different cell types involved (antigen-presenting cells, T-cells, and B-cells). The mechanisms and cellular basis of inflammation are considered, as are post-infection repair mechanisms, and pathologies of the immune system such as hypersensitivity, autoimmunity and transplantations, and immunodeficiency (both primary and secondary to other diseases).

scholarly journals Biology, Pathophysiological Role, and Clinical Implications of Exosomes: A Critical Appraisal

Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 99 ◽  
Author(s):  
Arif Jan ◽  
Safikur Rahman ◽  
Shahanavaj Khan ◽  
Sheikh Tasduq ◽  
Inho Choi
Keyword(s):  
Plasma Membranes ◽  
Molecular Mechanisms ◽  
Cell Types ◽  
Target Cells ◽  
Host Immune System ◽  
Messenger Rnas ◽  
Extracellular Milieu ◽  
Tumor Microenvironments ◽  
Physiological Processes ◽  
Antigen Presenting

Exosomes are membrane-enclosed entities of endocytic origin, which are generated during the fusion of multivesicular bodies (MVBs) and plasma membranes. Exosomes are released into the extracellular milieu or body fluids; this process was reported for mesenchymal, epithelial, endothelial, and different immune cells (B-cells and dendritic cells), and was reported to be correlated with normal physiological processes. The compositions and abundances of exosomes depend on their tissue origins and cell types. Exosomes range in size between 30 and 100 nm, and shuttle nucleic acids (DNA, messenger RNAs (mRNAs), microRNAs), proteins, and lipids between donor and target cells. Pathogenic microorganisms also secrete exosomes that modulate the host immune system and influence the fate of infections. Such immune-modulatory effect of exosomes can serve as a diagnostic biomarker of disease. On the other hand, the antigen-presenting and immune-stimulatory properties of exosomes enable them to trigger anti-tumor responses, and exosome release from cancerous cells suggests they contribute to the recruitment and reconstitution of components of tumor microenvironments. Furthermore, their modulation of physiological and pathological processes suggests they contribute to the developmental program, infections, and human diseases. Despite significant advances, our understanding of exosomes is far from complete, particularly regarding our understanding of the molecular mechanisms that subserve exosome formation, cargo packaging, and exosome release in different cellular backgrounds. The present study presents diverse biological aspects of exosomes, and highlights their diagnostic and therapeutic potentials.

Gap junction-mediated intercellular communication between DRG neurons and three target cell types

1998 ◽  
Vol 114 ◽  
pp. A1141
Author(s):  
H.S. Ennes ◽  
S.H. Young ◽  
J. Goliger ◽  
J. McRoberts ◽  
E.A. Mayer
Keyword(s):  
Gap Junction ◽  
Target Cell ◽  
Intercellular Communication ◽  
Cell Types ◽  
Drg Neurons

Intercellular communication via gap junction channels

1998 ◽  
Vol 45 (1) ◽  
pp. 55-65 ◽  
Author(s):  
Dieter F Hülser ◽  
Reiner Eckert ◽  
Uwe Irmer ◽  
Algimantas Krišciukaitis ◽  
Anja Mindermann ◽  
...  
Keyword(s):  
Gap Junction ◽  
Intercellular Communication ◽  
Gap Junction Channels

Adhesion of human T cells to antigen-presenting cells through SIRPβ2-CD47 interaction costimulates T-cell proliferation

Blood ◽  
2005 ◽  
Vol 105 (6) ◽  
pp. 2421-2427 ◽  
Author(s):  
Laura Piccio ◽  
William Vermi ◽  
Kent S. Boles ◽  
Anja Fuchs ◽  
Carey A. Strader ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Antigen Presenting Cells ◽  
Cell Types ◽  
Orphan Receptor ◽  
T Cell Proliferation ◽  
Central Nervous Systems ◽  
And Function ◽  
Antigen Presenting

AbstractSignal-regulatory proteins (SIRPs) are transmembrane glycoproteins belonging to the immunoglobulin (Ig) superfamily that are expressed in the immune and central nervous systems. SIRPα binds CD47 and inhibits the function of macrophages, dendritic cells, and granulocytes, whereas SIRPβ1 is an orphan receptor that activates the same cell types. A recently identified third member of the SIRP family, SIRPβ2, is as yet uncharacterized in terms of expression, specificity, and function. Here, we show that SIRPβ2 is expressed on T cells and activated natural killer (NK) cells and, like SIRPα, binds CD47, mediating cell-cell adhesion. Consequently, engagement of SIRPβ2 on T cells by CD47 on antigen-presenting cells results in enhanced antigen-specific T-cell proliferation.

Antagonistic effect of NK cells on alternatively activated monocytes: a contribution of NK cells to CTL generation

Blood ◽  
2002 ◽  
Vol 100 (12) ◽  
pp. 4049-4058 ◽  
Author(s):  
Anja B. Geldhof ◽  
Jo A. Van Ginderachter ◽  
YuanQing Liu ◽  
Wim Noël ◽  
Geert Raes ◽  
...  
Keyword(s):  
Immune System ◽  
Nk Cells ◽  
Antigen Presenting Cells ◽  
Tumor Rejection ◽  
Classical Type ◽  
Activated Monocytes ◽  
Antigen Presenting ◽  
Alternatively Activated

Natural killer (NK) cells fulfill essential accessory functions for the priming of antigen-specific cytotoxic T lymphocytes (CTLs). On the basis of a NKG2D-ligand–positive tumor model, we obtained results implicating NK-mediated regulatory as well as NK-mediated cytolytic activities in the initiation and persistence of CTL activity. Indeed, CD8+ T-cell–dependent tumor rejection requires NK cell function in vivo, because tumors will progress both on depletion of NK cells or in the absence of optimal NK activity. Here we provide evidence that the absence of NK cells during subcutaneous tumor growth will abrogate generation of antitumor CTL responses and that this process can be linked to the expansion of alternatively activated monocytes. Indeed, our in vitro studies demonstrate that in splenic cultures from NK-deficient tumor-bearing mice, lack of type 1–associated cytokines correlates with the presence of type 2 (alternatively activated) monocytes and the production of type 2 cytokines. Furthermore, these type 2 monocyte-containing splenic adherent populations potently suppress subsequent memory CTL restimulation. We evaluated the role of NK lytic effector functions in the efficient switch of the immune system toward classical (type 1) activation by including differentially activated monocytic populations as targets in cytotoxicity assays. The results indicate that the accessory function of NK cells depends partially on the ability of activated NK cells to preferentially engage type 2 antigen-presenting cells. Thus, when the immune system tends to be type 2 oriented, NK cells can drive an efficient type 2 → type 1 switch in the population of antigen-presenting cells to provide signaling for the generation of CTLs.

scholarly journals Selective Induction of Apoptosis in Antigen-Presenting Cells in Mice by Parapoxvirus ovis

2001 ◽  
Vol 75 (10) ◽  
pp. 4699-4704 ◽  
Author(s):  
Nicole Kruse ◽  
Olaf Weber
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Antigen Presenting Cells ◽  
T Cell Response ◽  
Survival Strategy ◽  
Short Intervals ◽  
Induction Of Apoptosis ◽  
Parapoxvirus Ovis ◽  
Antigen Presenting ◽  
Mouse System

ABSTRACT Viruses have evolved numerous mechanisms to avoid host immune reactions. Here we report a mechanism by which Parapoxvirus ovis (PPVO) interferes with antigen presentation. PPVO (orf virus) causes orf, an acute skin disease of sheep and goats worldwide. Importantly, PPVO can repeatedly infect its host in spite of a vigorous inflammatory and host immune response to the infection. We demonstrate in a mouse system that PPVO induces apoptosis in a significant number of antigen-presenting cells after intraperitoneal injection using the CD95 pathway, thus preventing a primary T-cell response. We also show that PPVO induces a compensatory activation of the immune system. Our results may help to explain the phenomenon that natural PPVO infections in sheep occur repeatedly even after short intervals. They also suggest that the combination of immunosuppressive and immunostimulatory mechanisms is an effective survival strategy that might be used in other viruses as well.

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