scholarly journals The roles of basophils in mediating the immune responses

2021 ◽  
Vol 19 ◽  
pp. 205873922110476
Author(s):  
Na Zhang ◽  
Ze-Ming Zhang ◽  
Xiao-Fei Wang
Keyword(s):  
Immune Responses ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Cell Sorting ◽  
Rapid Development ◽  
Host Immunity ◽  
Allergic Reactions ◽  
Effector Cells ◽  
High Affinity ◽  
High Affinity Ige Receptor

Basophils are the rarest blood cell population and have not been extensively studied. Our understanding of the functions of basophils is limited to their roles as the main effector cells in hypersensitivity reactions. Similar to mast cells, basophils express high-affinity IgE receptor (FcεRI), contain granules, and release hypersensitivity-associated mediators (such as histamine). The roles of basophils have not been fully elucidated; however, with the rapid development of monoclonal techniques, high-purity cell sorting techniques, and basophil-deficient mouse models, understanding of the functions and phenotypes of basophils has increased. This facilitates further investigations on the relationships between basophils and host immunity. Basophils are not only involved in mediating the generation of allergic reactions but also play important roles in immunomodulation and are responsible for the onset of infectious, allergic, and autoimmune diseases. In this review, we summarize the progress in understanding the roles of basophils in mediating immune responses with an emphasis on autoimmune diseases, particularly systemic lupus erythematosus and rheumatoid arthritis.

scholarly journals Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms

Viruses ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 762 ◽  
Author(s):  
Maria K. Smatti ◽  
Farhan S. Cyprian ◽  
Gheyath K. Nasrallah ◽  
Asmaa A. Al Thani ◽  
Ruba O. Almishal ◽  
...  
Keyword(s):  
Immune Responses ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Influenza A ◽  
Molecular Mechanisms ◽  
Viral Infections ◽  
Molecular Mimicry ◽  
Experimental Studies ◽  
Onset Time ◽  
Protective Effects

For a long time, viruses have been shown to modify the clinical picture of several autoimmune diseases, including type 1 diabetes (T1D), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Sjögren’s syndrome (SS), herpetic stromal keratitis (HSK), celiac disease (CD), and multiple sclerosis (MS). Best examples of viral infections that have been proposed to modulate the induction and development of autoimmune diseases are the infections with enteric viruses such as Coxsackie B virus (CVB) and rotavirus, as well as influenza A viruses (IAV), and herpesviruses. Other viruses that have been studied in this context include, measles, mumps, and rubella. Epidemiological studies in humans and experimental studies in animal have shown that viral infections can induce or protect from autoimmunopathologies depending on several factors including genetic background, host-elicited immune responses, type of virus strain, viral load, and the onset time of infection. Still, data delineating the clear mechanistic interaction between the virus and the immune system to induce autoreactivity are scarce. Available data indicate that viral-induced autoimmunity can be activated through multiple mechanisms including molecular mimicry, epitope spreading, bystander activation, and immortalization of infected B cells. Contrarily, the protective effects can be achieved via regulatory immune responses which lead to the suppression of autoimmune phenomena. Therefore, a better understanding of the immune-related molecular processes in virus-induced autoimmunity is warranted. Here we provide an overview of the current understanding of viral-induced autoimmunity and the mechanisms that are associated with this phenomenon.

scholarly journals Tertiary lymphoid organs in systemic autoimmune diseases:  pathogenic or protective?

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 196 ◽  
Author(s):  
William D. Shipman ◽  
Dragos C. Dasoveanu ◽  
Theresa T. Lu
Keyword(s):  
Rheumatoid Arthritis ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Lymphoid Organs ◽  
T And B Cells ◽  
Systemic Lupus ◽  
Disease Pathogenesis ◽  
Systemic Autoimmune Diseases ◽  
Effector Cells ◽  
Secondary Lymphoid Organs

Tertiary lymphoid organs are found at sites of chronic inflammation in autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. These organized accumulations of T and B cells resemble secondary lymphoid organs and generate autoreactive effector cells. However, whether they contribute to disease pathogenesis or have protective functions is unclear. Here, we discuss how tertiary lymphoid organs can generate potentially pathogenic cells but may also limit the extent of the response and damage in autoimmune disease.

scholarly journals Mast Cells as Important Regulators in Autoimmunity and Cancer Development

2021 ◽  
Vol 9 ◽  
Author(s):  
Christine N. Noto ◽  
Stella G. Hoft ◽  
Richard J. DiPaolo
Keyword(s):  
Mast Cells ◽  
Immune Responses ◽  
Autoimmune Diseases ◽  
Inflammatory Mediators ◽  
T Regulatory Cells ◽  
Effector Cells ◽  
T Effector Cells ◽  
Tumor Microenvironments ◽  
Immunological Effect ◽  
Anti Inflammatory

Mast cells are an essential part of the immune system and are best known as important modulators of allergic and anaphylactic immune responses. Upon activation, mast cells release a multitude of inflammatory mediators with various effector functions that can be both protective and damage-inducing. Mast cells can have an anti-inflammatory or pro-inflammatory immunological effect and play important roles in regulating autoimmune diseases including rheumatoid arthritis, type 1 diabetes, and multiple sclerosis. Importantly, chronic inflammation and autoimmunity are linked to the development of specific cancers including pancreatic cancer, prostate cancer, colorectal cancer, and gastric cancer. Inflammatory mediators released from activated mast cells regulate immune responses and promote vascular permeability and the recruitment of immune cells to the site of inflammation. Mast cells are present in increased numbers in tissues affected by autoimmune diseases as well as in tumor microenvironments where they co-localize with T regulatory cells and T effector cells. Mast cells can regulate immune responses by expressing immune checkpoint molecules on their surface, releasing anti-inflammatory cytokines, and promoting vascularization of solid tumor sites. As a result of these immune modulating activities, mast cells have disease-modifying roles in specific autoimmune diseases and cancers. Therefore, determining how to regulate the activities of mast cells in different inflammatory and tumor microenvironments may be critical to discovering potential therapeutic targets to treat autoimmune diseases and cancer.

scholarly journals IgG glycosylation in autoimmune diseases

2018 ◽  
Vol 72 ◽  
pp. 975-990 ◽  
Author(s):  
Kamila Kozłowska ◽  
Magdalena Rydlewska ◽  
Marta Ząbczyńska ◽  
Ewa Pocheć
Keyword(s):  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Glycosylation Site ◽  
Glycan Structure ◽  
Post Translational Modification ◽  
Inflammatory Reactions ◽  
Effector Cells ◽  
Suppression Of Immune Response ◽  
Igg Glycosylation

Immunoglobulin G (IgG) is the most abundant glycoprotein in human serum. All IgG subclasses have a single-conserved N-linked glycosylation site at Asn297 of the heavy chain and 10–30% of IgGs are N-glycosylated also in a Fab region. N-glycans of Fc are sialylated and fucosylated biantennary complex-type structures. Glycosylation plays a key role in antibody function, and IgG N-glycans are essential for the proper activity of the immune system. Fc glycans are important for IgG effector functions, whereas Fab oligosaccharides modulate antigen binding. Glycosylation changes of IgG are associated with the development of various human diseases, including autoimmune states. The modification of one sugar moiety in N-glycan structure may result in the stimulation or suppression of immune response. The lack of core fucose leads to the enhancement of pro-inflammatory activity, whereas an increase of sialylation determines immunosuppressive properties of IgG. The contribution of IgG Fc glycosylation changes has been demonstrated in the pathogenesis of rheumatoid arthritis, lupus erythematosus and Crohn’s disease. A decrease in IgG galactosylation and sialylation, found in these diseases, activates effector cells and triggers inflammatory reactions. A detailed analysis of changes in IgG glycosylation and their effects on the development of autoimmune diseases is important in the treatment of these diseases. IgGs with modified α2,6-sialylation are used as therapeutic antibodies with anti-inflammatory properties. Numerous studies on IgG glycosylation have provided evidence of the role of this post-translational modification in the proper functioning of antibodies and the importance of changes in the structure of IgG glycans, mainly incomplete galactosylation and desialylation, in the pathogenesis of many diseases. The continuation of these studies may contribute to explaining the mechanisms of autoimmunity that is still poorly understood.

High-Affinity IgE Receptor Fc Epsilon Rl Expression in Allergic Reactions

1997 ◽  
Vol 113 (1-3) ◽  
pp. 376-378 ◽  
Author(s):  
J.A. Grant ◽  
M. Humbert ◽  
L. Taborda-Barata ◽  
B.S. Sihra ◽  
O.M. Kon ◽  
...  
Keyword(s):  
Allergic Reactions ◽  
Ige Receptor ◽  
High Affinity ◽  
High Affinity Ige Receptor

scholarly journals Innate immune responses to rhinovirus are reduced by the high-affinity IgE receptor in allergic asthmatic children

2012 ◽  
Vol 130 (2) ◽  
pp. 489-495 ◽  
Author(s):  
Sandy R. Durrani ◽  
Daniel J. Montville ◽  
Allison S. Pratt ◽  
Sanjukta Sahu ◽  
Mark K. DeVries ◽  
...  
Keyword(s):  
Immune Responses ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Ige Receptor ◽  
Asthmatic Children ◽  
High Affinity ◽  
Allergic Asthmatic ◽  
High Affinity Ige Receptor

scholarly journals Strategies to Use Nanoparticles to Generate CD4 and CD8 Regulatory T Cells for the Treatment of SLE and Other Autoimmune Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
David A. Horwitz ◽  
Sean Bickerton ◽  
Antonio La Cava
Keyword(s):  
T Cells ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
T Regulatory Cells ◽  
Inflammatory Diseases ◽  
Antigen Presenting Cells ◽  
Protective Effects ◽  
Effector Cells ◽  
Self Tolerance ◽  
Antigen Presenting

Autoimmune diseases are disorders of immune regulation where the mechanisms responsible for self-tolerance break down and pathologic T cells overcome the protective effects of T regulatory cells (Tregs) that normally control them. The result can be the initiation of chronic inflammatory diseases. Systemic lupus erythematosus (SLE) and other autoimmune diseases are generally treated with pharmacologic or biological agents that have broad suppressive effects. These agents can halt disease progression, yet rarely cure while carrying serious adverse side effects. Recently, nanoparticles have been engineered to correct homeostatic regulatory defects and regenerate therapeutic antigen-specific Tregs. Some approaches have used nanoparticles targeted to antigen presenting cells to switch their support from pathogenic T cells to protective Tregs. Others have used nanoparticles targeted directly to T cells for the induction and expansion of CD4+ and CD8+ Tregs. Some of these T cell targeted nanoparticles have been formulated to act as tolerogenic artificial antigen presenting cells. This article discusses the properties of these various nanoparticle formulations and the strategies to use them in the treatment of autoimmune diseases. The restoration and maintenance of Treg predominance over effector cells should promote long-term autoimmune disease remission and ultimately prevent them in susceptible individuals.

scholarly journals The IL-2 Defect in Systemic Lupus Erythematosus Disease Has an Expansive Effect on Host Immunity

2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
Linda A. Lieberman ◽  
George C. Tsokos
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune Responses ◽  
Lupus Erythematosus ◽  
Cell Function ◽  
Host Immunity ◽  
Systemic Lupus Erythematosus Disease ◽  
Systemic Lupus ◽  
Host Immune Responses ◽  
Activation Induced Cell Death ◽  
Immune Defects

IL-2 production is decreased in systemic lupus erythematosus (SLE) patients and affects T cell function and other aspects of host immunity. Transcription factors regulating IL-2 production behave aberrantly in SLE T cells. In addition to IL-2 dysregulation, other IL-2 family members (IL-15 and IL-21) are abnormally expressed in SLE. Decreased IL-2 production in SLE patients leads to many immune defects such as decreasedTregproduction, decreased activation-induced cell death (AICD), and decreased cytotoxicity. IL-2 deficiency results in systemic dysregulation of host immune responses in patients suffering from SLE disease.

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