scholarly journals The Adipocyte and Adaptive Immunity

2020 ◽  
Vol 11 ◽  
Author(s):  
Jianfeng Song ◽  
Tuo Deng
Keyword(s):  
T Cells ◽  
B Cell ◽  
Adaptive Immunity ◽  
Mhc Class Ii ◽  
Inflammatory Diseases ◽  
Adaptive Immune Response ◽  
Adaptive Immune ◽  
Proliferation And Differentiation ◽  
Antigen Presenting ◽  
Mhc Class Ii Molecules

Not only do Adipocytes have energy storage and endocrine functions, but they also play an immunological role. Adipocytes are involved in adaptive immunity to mediate the pathological processes of a variety of chronic inflammatory diseases and autoimmune syndromes. The adaptive immune response consists of T cell-mediated cellular immunity and B cell-mediated humoral immunity. Obese adipocytes overexpress MHC class II molecules and costimulators to act as antigen-presenting cells (APCs) and promote the activation of CD4+ T cells. In addition, various adipokines secreted by adipocytes regulate the proliferation and differentiation of T cells. Adipokines are also involved in B cell generation, development, activation, and antibody production. Therefore, adipocytes play an important role in B cell-mediated adaptive immunity. This review describes how adipocytes participate in adaptive immunity from the perspective of T cells and B cells, and discusses their role in the pathogenesis of various diseases.

scholarly journals The importance of the back–signal from T cells into antigen–presenting cells in determining susceptibility to parasites

1997 ◽  
Vol 352 (1359) ◽  
pp. 1327-1330 ◽  
Author(s):  
Brigitte Müller ◽  
Avrion Mitchison
Keyword(s):  
T Cells ◽  
Immune Responses ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Activated T Cells ◽  
Ifn Gamma ◽  
Parasite Infections ◽  
Antigen Presenting ◽  
Mhc Class Ii Genes ◽  
Mhc Class Ii Molecules

It has long been known that certain MHC class II genes can dominantly suppress immune responses and so increase susceptibility to parasite infections, but the mechanism has been unclear. Recent work has revealed one way in which this form of suppression may operate through gating by MHC class II molecules of the back–signal from activated T cells into macrophages. The two known suppressive genes of the mouse are expressed in macrophages more extensively than are other class II genes. This is asscociated with suppresion of IL–4 production resulting, we infer, from overproduction in the macrophages of IL–12, the counter–cytokine to IL–4. The lack of IL–4 may itself be immunosuppressive, even for Th2 responses, and excess IL–12 can overinduce the antiproliferative cytokine IFN–gamma. Although this mechanism requires further substantiation, we believe that it offers a reasonable answer to an old conundrum.

scholarly journals Glatiramer acetate immune modulates B-cell antigen presentation in treatment of MS

2020 ◽  
Vol 7 (3) ◽  
pp. e698 ◽  
Author(s):  
Darius Häusler ◽  
Zivar Hajiyeva ◽  
Jan W. Traub ◽  
Scott S. Zamvil ◽  
Patrice H. Lalive ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Antigen Presentation ◽  
Glatiramer Acetate ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Cell Antigen ◽  
Antigen Presenting

ObjectiveWe examined the effect of glatiramer acetate (GA) on B-cell maturation, differentiation, and antigen presentation in MS and experimental autoimmune encephalomyelitis (EAE).MethodsA cross-sectional study of blood samples from 20 GA-treated and 18 untreated patients with MS was performed by flow cytometry; 6 GA-treated patients with MS were analyzed longitudinally. GA-mediated effects on B-cell antigen-presenting function were investigated in EAE, or, alternatively, B cells were treated with GA in vitro using vehicle as a control.ResultsIn MS, GA diminished transitional B-cell and plasmablast frequency, downregulated CD69, CD25, and CD95 expression, and decreased TNF-α production, whereas IL-10 secretion and MHC Class II expression were increased. In EAE, we observed an equivalent dampening of proinflammatory B-cell properties and an enhanced expression of MHC Class II. When used as antigen-presenting cells for activation of naive T cells, GA-treated B cells promoted development of regulatory T cells, whereas proinflammatory T-cell differentiation was diminished.ConclusionsGA immune modulates B-cell function in EAE and MS and efficiently interferes with pathogenic B cell–T cell interaction.

IKKα in the regulation of inflammation and adaptive immunity

2007 ◽  
Vol 35 (2) ◽  
pp. 270-272 ◽  
Author(s):  
T. Lawrence ◽  
M. Bebien
Keyword(s):  
Adaptive Immunity ◽  
Adaptive Immune Response ◽  
Nuclear Factor Κb ◽  
Catalytic Subunits ◽  
Adaptive Immune ◽  
Inflammatory Stimuli ◽  
Important Regulator ◽  
Beneficial Response ◽  
Antigen Presenting ◽  
Inflammatory Signalling

Inflammation is a beneficial response to insult or injury which plays an important role in orchestrating the adaptive immune response. The resolution of acute inflammation is an active process that involves the release of anti-inflammatory mediators and the termination of pro-inflammatory signalling pathways coincident with leucocyte apoptosis and phagocytic clearance and the migration of antigen-presenting cells from the site of inflammation to the local lymphatic tissue. The latter process is required for the development of adaptive immunity and immunological memory. The NF-κB (nuclear factor κB) pathway is an important regulator of inflammation and immunity; NF-κB activation is controlled by IKK [IκB (inhibitor of NF-κB) kinase] complex, which regulates NF-κB activation in response to pro-inflammatory stimuli. The IKK complex has two catalytic subunits, IKKα and IKKβ; recent research shows that these highly homologous kinases have distinct roles in inflammation and adaptive immunity. Here, we discuss the emerging roles for IKKα in the tight regulation of inflammation and the development of adaptive immune responses.

scholarly journals Adaptive Immunity: The Role of Toll-Like Receptors

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yamaguchi R ◽  
◽  
Sakamoto A ◽  
Yamaguchi R ◽  
Haraguchi M ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Autoimmune Diseases ◽  
Adaptive Immunity ◽  
Th17 Cells ◽  
Adaptive Immune Response ◽  
Toll Like Receptors ◽  
Adaptive Immune ◽  
Interleukin 23

The central mediators of the adaptive immune response are T cells. The clonal expansion of T cells required for adaptive immunity results from the innate immune response, which is triggered by the stimulation of Toll-Like Receptors (TLRs). The adaptive immune response can cause autoimmune diseases, and Th17 cells are known to contribute to several autoimmune diseases. Pathogenic Th17 cells are induced by Interleukin 23 (IL-23) and IL-1Β. Resiquimod (a TLR7/8 agonist) significantly enhances IL-23 production by human macrophages, and lipopolysaccharide (a TLR4 agonist) slightly enhances it. Interestingly, IL-23 levels are significantly attenuated after sequential stimulation with lipopolysaccharide and resiquimod, indicating cross-talk between the TLR4 and TLR7/8 signaling pathways. In this review, we discuss the pivotal role of TLRs in triggering innate immunity and inducing adaptive immunity, leading to autoimmune diseases.

scholarly journals The Interplay between Bluetongue Virus Infections and Adaptive Immunity

Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1511
Author(s):  
Daniel Rodríguez-Martín ◽  
Andrés Louloudes-Lázaro ◽  
Miguel Avia ◽  
Verónica Martín ◽  
José M. Rojas ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Adaptive Immunity ◽  
Bluetongue Virus ◽  
Viral Infections ◽  
Adaptive Immune Response ◽  
Γδ T Cells ◽  
Neutralizing Antibody ◽  
Immune Mechanisms ◽  
Adaptive Immune

Viral infections have long provided a platform to understand the workings of immunity. For instance, great strides towards defining basic immunology concepts, such as MHC restriction of antigen presentation or T-cell memory development and maintenance, have been achieved thanks to the study of lymphocytic choriomeningitis virus (LCMV) infections. These studies have also shaped our understanding of antiviral immunity, and in particular T-cell responses. In the present review, we discuss how bluetongue virus (BTV), an economically important arbovirus from the Reoviridae family that affects ruminants, affects adaptive immunity in the natural hosts. During the initial stages of infection, BTV triggers leucopenia in the hosts. The host then mounts an adaptive immune response that controls the disease. In this work, we discuss how BTV triggers CD8+ T-cell expansion and neutralizing antibody responses, yet in some individuals viremia remains detectable after these adaptive immune mechanisms are active. We present some unpublished data showing that BTV infection also affects other T cell populations such as CD4+ T-cells or γδ T-cells, as well as B-cell numbers in the periphery. This review also discusses how BTV evades these adaptive immune mechanisms so that it can be transmitted back to the arthropod host. Understanding the interaction of BTV with immunity could ultimately define the correlates of protection with immune mechanisms that would improve our knowledge of ruminant immunology.

Double positive CD4+CD8+ T cells are part of the adaptive immune response against Candida albicans

2019 ◽  
Vol 80 (12) ◽  
pp. 999-1005 ◽  
Author(s):  
Barbara Misme-Aucouturier ◽  
Adel Touahri ◽  
Marjorie Albassier ◽  
Francine Jotereau ◽  
Patrice Le Pape ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Candida Albicans ◽  
Cd8 T Cells ◽  
Adaptive Immune Response ◽  
Double Positive ◽  
Adaptive Immune
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