scholarly journals Diet and Hygiene in Modulating Autoimmunity During the Pandemic Era

2022 ◽  
Vol 12 ◽  
Author(s):  
Leila Abdelhamid ◽  
Xin M. Luo
Keyword(s):  
Immune System ◽  
Environmental Factors ◽  
Immune Responses ◽  
Host Defense ◽  
Lupus Erythematosus ◽  
Inflammatory Responses ◽  
Immune Recognition ◽  
Systemic Autoimmunity ◽  
Hygiene Measures ◽  
Autoimmune Conditions

The immune system is an efficiently toned machinery that discriminates between friends and foes for achieving both host defense and homeostasis. Deviation of immune recognition from foreign to self and/or long-lasting inflammatory responses results in the breakdown of tolerance. Meanwhile, educating the immune system and developing immunological memory are crucial for mounting defensive immune responses while protecting against autoimmunity. Still to elucidate is how diverse environmental factors could shape autoimmunity. The emergence of a world pandemic such as SARS-CoV-2 (COVID-19) not only threatens the more vulnerable individuals including those with autoimmune conditions but also promotes an unprecedented shift in people’s dietary approaches while urging for extraordinary hygiene measures that likely contribute to the development or exacerbation of autoimmunity. Thus, there is an urgent need to understand how environmental factors modulate systemic autoimmunity to better mitigate the incidence and or severity of COVID-19 among the more vulnerable populations. Here, we discuss the effects of diet (macronutrients and micronutrients) and hygiene (the use of disinfectants) on autoimmunity with a focus on systemic lupus erythematosus.

Human MUC1 Mucin: A Multifaceted Glycoprotein

2000 ◽  
Vol 15 (4) ◽  
pp. 343-356 ◽  
Author(s):  
S. von Mensdorff-Pouilly ◽  
F.G.M. Snijdewint ◽  
A.A. Verstraeten ◽  
R.H.M. Verheijen ◽  
P. Kenemans
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Cancer Patients ◽  
Cancer Progression ◽  
Early Stage ◽  
Immune Recognition ◽  
Breast Cancer Patients ◽  
Phase I Clinical Trials ◽  
Muc1 Mucin ◽  
Human Muc1

Human MUC1 mucin, a membrane-bound glycoprotein, is a major component of the ductal cell surface of normal glandular cells. MUC1 is overexpressed and aberrantly glycosylated in carcinoma cells. The role MUC1 plays in cancer progression represents two sides of one coin: on the one hand, loss of polarity and overexpression of MUC1 in cancer cells interferes with cell adhesion and shields the tumor cell from immune recognition by the cellular arm of the immune system, thus favoring metastases; on the other hand, MUC1, in essence a self-antigen, is displaced and altered in malignancy and induces immune responses. Tumor-associated MUC1 has short carbohydrate sidechains and exposed epitopes on its peptide core; it gains access to the circulation and comes into contact with the immune system provoking humoral and cellular immune responses. Natural antibodies to MUC1 present in the circulation of cancer patients may be beneficial to the patient by restricting tumor growth and dissemination: early stage breast cancer patients with a humoral response to MUC1 have a better disease-specific survival. Several MUC1 peptide vaccines, differing in vectors, carrier proteins and adjuvants, have been tested in phase I clinical trials. They are capable of inducing predominantly humoral responses to the antigen, but evidence that these immune responses may be effective against the tumor in humans is still scarce.

Immune and Inflammatory Responses to Stroke: Good Or Bad?

2008 ◽  
Vol 3 (4) ◽  
pp. 254-265 ◽  
Author(s):  
P. A. McCombe ◽  
S. J. Read
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Immune Responses ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Therapeutic Option ◽  
Regulatory Lymphocytes ◽  
The Brain ◽  
Pro Inflammatory Cytokines

Inflammatory and immune responses play important roles following ischaemic stroke. Inflammatory responses contribute to damage and also contribute to repair. Injury to tissue triggers an immune response. This is initiated through activation of the innate immune system. In stroke there is microglial activation. This is followed by an influx of lymphocytes and macrophages into the brain, triggered by production of pro-inflammatory cytokines. This inflammatory response contributes to further tissue injury. There is also a systemic immune response to stroke, and there is a degree of immunosuppression that may contribute to the stroke patient's risk of infection. This immunosuppressive response may also be protective, with regulatory lymphocytes producing cytokines and growth factors that are neuroprotective. The specific targets of the immune response after stroke are not known, and the details of the immune and inflammatory responses are only partly understood. The role of inflammation and immune responses after stroke is twofold. The immune system may contribute to damage after stroke, but may also contribute to repair processes. The possibility that some of the immune response after stroke may be neuroprotective is exciting and suggests that deliberate enhancement of these responses may be a therapeutic option.

scholarly journals Loss of the lupus autoantigen Ro52/Trim21 induces tissue inflammation and systemic autoimmunity by disregulating the IL-23–Th17 pathway

2009 ◽  
Vol 206 (8) ◽  
pp. 1661-1671 ◽  
Author(s):  
Alexander Espinosa ◽  
Valerie Dardalhon ◽  
Susanna Brauner ◽  
Aurelie Ambrosi ◽  
Rowan Higgs ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Tissue Injury ◽  
Negative Regulator ◽  
Systemic Lupus ◽  
Tissue Inflammation ◽  
Enhanced Production ◽  
Systemic Autoimmunity ◽  
Autoimmune Conditions ◽  
Important Negative Regulator ◽  
Genetic Deletion

Ro52/Trim21 is targeted as an autoantigen in systemic lupus erythematosus and Sjögren's syndrome. Polymorphisms in the Ro52 gene have been linked to these autoimmune conditions, but the molecular mechanism by which Ro52 may promote development of systemic autoimmune diseases has not been explored. To address this issue, we generated Ro52-null mice (Ro52−/−), which appear phenotypically normal if left unmanipulated. However, Ro52−/− mice develop severe dermatitis extending from the site of tissue injury induced by ear tags. The affected mice further develop several signs of systemic lupus with hypergammaglobulinemia, autoantibodies to DNA, proteinuria, and kidney pathology. Ro52, which was recently identified as an E3 ligase, mediates ubiquitination of several members of the interferon regulatory factor (IRF) family, and the Ro52-deficient mice have an enhanced production of proinflammatory cytokines that are regulated by the IRF transcription factors, including cytokines involved in the Th17 pathway (interleukin [IL] 6, IL-12/IL-23p40, and IL-17). Loss of IL-23/IL-17 by genetic deletion of IL-23/p19 in the Ro52−/− mice conferred protection from skin disease and systemic autoimmunity. These data reveal that the lupus-associated Ro52 protein is an important negative regulator of proinflammatory cytokine production, and they provide a mechanism by which a defective Ro52 function can lead to tissue inflammation and systemic autoimmunity through the IL-23–Th17 pathway.

scholarly journals Intestinal macrophages in mucosal immunity and their role in systemic lupus erythematosus disease

Lupus ◽  
2018 ◽  
Vol 27 (12) ◽  
pp. 1898-1902 ◽  
Author(s):  
F Pan ◽  
W Tang ◽  
Z Zhou ◽  
G Gilkeson ◽  
R Lang ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune Responses ◽  
Lupus Erythematosus ◽  
Inflammatory Responses ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Systemic Lupus ◽  
Innate Immune Signaling ◽  
Immune Signaling Pathway

Monocytes play an important role in inducing host systemic immunity against invading pathogens and inflammatory responses. After activation, monocytes migrate to tissue sites, where they initiate both innate and adaptive immune responses, and become macrophages. Although mucosal macrophages produce inflammatory cytokines in response to pathogens, the perturbations in innate immune signaling pathway have been implicated in autoimmune diseases such as systemic lupus erythematosus (SLE). In this review, we focus on the role of human macrophages in intestinal innate immune responses, homeostasis, and SLE disease. We further discuss sex differences in the intestinal macrophages and their role in the physiology and pathogenesis of SLE.

scholarly journals The immunorecognition, subcellular compartmentalization, and physicochemical properties of nucleic acid nanoparticles can be controlled by composition modification

2020 ◽  
Vol 48 (20) ◽  
pp. 11785-11798
Author(s):  
Morgan Brittany Johnson ◽  
Justin R Halman ◽  
Daniel K Miller ◽  
Joseph S Cooper ◽  
Emil F Khisamutdinov ◽  
...  
Keyword(s):  
Nucleic Acid ◽  
Immune Responses ◽  
Nucleic Acids ◽  
Targeted Delivery ◽  
Inflammatory Responses ◽  
Diagnostic Tools ◽  
Immune Recognition ◽  
Composition Modification ◽  
Target Molecules ◽  
Subcellular Compartmentalization

Abstract Nucleic acid nanoparticles (NANPs) have become powerful new platforms as therapeutic and diagnostic tools due to the innate biological ability of nucleic acids to identify target molecules or silence genes involved in disease pathways. However, the clinical application of NANPs has been limited by factors such as chemical instability, inefficient intracellular delivery, and the triggering of detrimental inflammatory responses following innate immune recognition of nucleic acids. Here, we have studied the effects of altering the chemical composition of a circumscribed panel of NANPs that share the same connectivity, shape, size, charge and sequences. We show that replacing RNA strands with either DNA or chemical analogs increases the enzymatic and thermodynamic stability of NANPs. Furthermore, we have found that such composition changes affect delivery efficiency and determine subcellular localization, effects that could permit the targeted delivery of NANP-based therapeutics and diagnostics. Importantly, we have determined that altering NANP composition can dictate the degree and mechanisms by which cell immune responses are initiated. While RNA NANPs trigger both TLR7 and RIG-I mediated cytokine and interferon production, DNA NANPs stimulate minimal immune activation. Importantly, incorporation of 2′F modifications abrogates RNA NANP activation of TLR7 but permits RIG-I dependent immune responses. Furthermore, 2′F modifications of DNA NANPs significantly enhances RIG-I mediated production of both proinflammatory cytokines and interferons. Collectively this indicates that off-target effects may be reduced and/or desirable immune responses evoked based upon NANPs modifications. Together, our studies show that NANP composition provides a simple way of controlling the immunostimulatory potential, and physicochemical and delivery characteristics, of such platforms.

scholarly journals Immune Therapy in GI Malignancies: A Review

2015 ◽  
Vol 33 (16) ◽  
pp. 1745-1753 ◽  
Author(s):  
Judy Wang ◽  
Kim A. Reiss ◽  
Rina Khatri ◽  
Elizabeth Jaffee ◽  
Dan Laheru
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Immune Suppression ◽  
Immune Therapy ◽  
Immune Recognition ◽  
Systemic Factors ◽  
Tumor Environment ◽  
The Difference ◽  
Complex Relationships

The balance between tumor-promoting and tumor-suppressing immune responses and the difference between them ultimately determine whether a cancer escapes immune recognition mechanisms. Defining the complex relationships between the tumor itself, the tumor environment, and the immune system has been critical in facilitating the development of successful immunotherapies. This review explores the role of oncogenes in inducing cancer-associated inflammation, the local and systemic factors that lead to immune suppression, and immunotherapy approaches to overcome immune privilege.

scholarly journals General factors that influence the immune responses in children

2020 ◽  
Vol 185 ◽  
pp. 03013
Author(s):  
Eun Hee Ha
Keyword(s):  
Immune System ◽  
Environmental Factors ◽  
Immune Responses ◽  
Cytokine Production ◽  
Research Paper ◽  
Future Research ◽  
Immunoglobulin Production

The research paper is written with the aim to identify different factors that influence children’s immune responses. Five theories are explored on children’s susceptibility to certain diseases and their lack of susceptibility to others. Aspects that are explored in this paper are children’s levels of immunoglobulin production, their cytokine production amount, their underdevelopment of receptors, their asymptomatic nature to certain diseases, and environmental factors. Through exploring different studies on child immunity, the paper concludes that the susceptibility of children to diseases largely depends on the type of disease and the individual’s immune system. Future research is clearly required to identify a smaller scope of the factors that influence children’s immune responses to provide a more detailed reasoning in the causes of children’s proneness to certain diseases and their lack of susceptibility in others.

Trigger factors of cutaneous lupus erythematosus: a review of current literature

Lupus ◽  
2017 ◽  
Vol 26 (8) ◽  
pp. 791-807 ◽  
Author(s):  
J Szczęch ◽  
D Samotij ◽  
V P Werth ◽  
A Reich
Keyword(s):  
Environmental Factors ◽  
Lupus Erythematosus ◽  
Cutaneous Lupus Erythematosus ◽  
Scientific Data ◽  
Convincing Evidence ◽  
Trigger Factors ◽  
Relevant Role ◽  
Autoimmune Conditions ◽  
Cutaneous Lupus

It is currently believed that autoimmune conditions are triggered and aggravated by a variety of environmental factors such as cigarette smoking, infections, ultraviolet light or chemicals, as well as certain medications and vaccines in genetically susceptible individuals. Recent scientific data have suggested a relevant role of these factors not only in systemic lupus erythematosus, but also in cutaneous lupus erythematosus (CLE). A variety of environmental factors have been proposed as initiators and exacerbators of this disease. In this review we focused on those with the most convincing evidence, emphasizing the role of drugs in CLE. Using a combined search strategy of the MEDLINE and CINAHL databases the following trigger factors and/or exacerbators of CLE have been identified and described: drugs, smoking, neoplasms, ultraviolet radiation and radiotherapy. In order to give a practical insight we emphasized the role of drugs from various groups and classes in CLE. We also aimed to present a short clinical profile of patients with lesions induced by various drug classes.

scholarly journals Bim suppresses the development of SLE by limiting myeloid inflammatory responses

2017 ◽  
Vol 214 (12) ◽  
pp. 3753-3773 ◽  
Author(s):  
FuNien Tsai ◽  
Philip J. Homan ◽  
Hemant Agrawal ◽  
Alexander V. Misharin ◽  
Hiam Abdala-Valencia ◽  
...  
Keyword(s):  
Lupus Erythematosus ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Adaptor Protein ◽  
Type I ◽  
Apoptotic Pathway ◽  
Systemic Autoimmunity ◽  
Molecular Rheostat ◽  
The Guardian

The Bcl-2 family is considered the guardian of the mitochondrial apoptotic pathway. We demonstrate that Bim acts as a molecular rheostat by controlling macrophage function not only in lymphoid organs but also in end organs, thereby preventing the break in tolerance. Mice lacking Bim in myeloid cells (LysMCreBimfl/fl) develop a systemic lupus erythematosus (SLE)–like disease that mirrors aged Bim−/− mice, including loss of marginal zone macrophages, splenomegaly, lymphadenopathy, autoantibodies (including anti-DNA IgG), and a type I interferon signature. LysMCreBimfl/fl mice exhibit increased mortality attributed to glomerulonephritis (GN). Moreover, the toll-like receptor signaling adaptor protein TRIF (TIR-domain–containing adapter-inducing interferon-β) is essential for GN, but not systemic autoimmunity in LysMCreBimfl/fl mice. Bim-deleted kidney macrophages exhibit a novel transcriptional lupus signature that is conserved within the gene expression profiles from whole kidney biopsies of patients with SLE. Collectively, these data suggest that the Bim may be a novel therapeutic target in the treatment of SLE.

Control of Immunity by the Microbiota

2021 ◽  
Vol 39 (1) ◽  
pp. 449-479
Author(s):  
Eduard Ansaldo ◽  
Taylor K. Farley ◽  
Yasmine Belkaid
Keyword(s):  
T Cells ◽  
Immune System ◽  
Immune Responses ◽  
Microbial Communities ◽  
Adaptive Immunity ◽  
Immune Recognition ◽  
T Helper ◽  
Cell Responses ◽  
Temporal Windows

The immune system has coevolved with extensive microbial communities living on barrier sites that are collectively known as the microbiota. It is increasingly clear that microbial antigens and metabolites engage in a constant dialogue with the immune system, leading to microbiota-specific immune responses that occur in the absence of inflammation. This form of homeostatic immunity encompasses many arms of immunity, including B cell responses, innate-like T cells, and conventional T helper and T regulatory responses. In this review we summarize known examples of innate-like T cell and adaptive immunity to the microbiota, focusing on fundamental aspects of commensal immune recognition across different barrier sites. Furthermore, we explore how this cross talk is established during development, emphasizing critical temporal windows that establish long-term immune function. Finally, we highlight how dysregulation of immunity to the microbiota can lead to inflammation and disease, and we pinpoint outstanding questions and controversies regarding immune system–microbiota interactions.

Sign in / Sign up

Export Citation Format

Share Document