scholarly journals Subacute thyroiditis as evidence of SARS-CoV2 related autoimmune disorders and case descriptions

2021 ◽  
Keyword(s):  
Immune Response ◽  
Autoimmune Diseases ◽  
Viral Infection ◽  
Autoimmune Disorders ◽  
Subacute Thyroiditis ◽  
Previous Experience ◽  
Inflammatory Condition ◽  
Inflammatory Mechanism ◽  
Inflammatory Immune Response

Context: Subacute thyroiditis has been classified as an auto inflammatory condition and occurs mainly due to a viral infection. According to the pathogenesis of SARS-CoV2 infection, which is mainly based on the uncontrolled inflammatory immune response, several studies have investigated the possible association between SARS-CoV2 and subacute thyroiditis. In this regard, we aimed to review and organize these studies. Evidence Acquisition: First, we observed and provided evidence on the possible roles and mechanisms of SARS-CoV2 in inflammatory and autoimmune diseases, and then we discussed the findings on the association between subacute thyroiditis and SARS-CoV2 infection. Results: Regarding other autoimmune and inflammatory disorders, together with previous experience on the role of viruses in the pathogenesis of subacute thyroiditis, as well as studies on the inflammatory mechanism of SARS-CoV2 infection, support this hypothesis that SARS-CoV2 may initiate subacute thyroiditis. Conclusions: Evidence so far suggests that subacute thyroiditis should be considered as a later symptom of covid-19.

scholarly journals Epigenetic Changes in the Regulation of Nicotiana tabacum Response to Cucumber Mosaic Virus Infection and Symptom Recovery through Single-Base Resolution Methylomes

Viruses ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 402 ◽  
Author(s):  
Chenguang Wang ◽  
Chaonan Wang ◽  
Wenjie Xu ◽  
Jingze Zou ◽  
Yanhong Qiu ◽  
...  
Keyword(s):  
Immune Response ◽  
Nicotiana Tabacum ◽  
Viral Infection ◽  
Cucumber Mosaic Virus ◽  
Mosaic Virus ◽  
Developmental Stages ◽  
Reduced Representation ◽  
Reduced Representation Bisulfite Sequencing ◽  
Symptom Recovery

Plants have evolved multiple mechanisms to respond to viral infection. These responses have been studied in detail at the level of host immune response and antiviral RNA silencing (RNAi). However, the possibility of epigenetic reprogramming has not been thoroughly investigated. Here, we identified the role of DNA methylation during viral infection and performed reduced representation bisulfite sequencing (RRBS) on tissues of Cucumber mosaic virus (CMV)-infected Nicotiana tabacum at various developmental stages. Differential methylated regions are enriched with CHH sequence contexts, 80% of which are located on the gene body to regulate gene expression in a temporal style. The methylated genes depressed by methyltransferase inhibition largely overlapped with methylated genes in response to viral invasion. Activation in the argonaute protein and depression in methyl donor synthase revealed the important role of dynamic methylation changes in modulating viral clearance and resistance signaling. Methylation-expression relationships were found to be required for the immune response and cellular components are necessary for the proper defense response to infection and symptom recovery.

scholarly journals Interferon-Stimulated Genes as Enhancers of Antiviral Innate Immune Signaling

2017 ◽  
Vol 10 (2) ◽  
pp. 85-93 ◽  
Author(s):  
Keaton M. Crosse ◽  
Ebony A. Monson ◽  
Michael R. Beard ◽  
Karla J. Helbig
Keyword(s):  
Immune Response ◽  
Viral Infection ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Regulatory Factor ◽  
Interferon Stimulated Genes ◽  
Innate Immune Signaling ◽  
Recent Advancement ◽  
Antiviral Function

The ability of a host to curb a viral infection is heavily reliant on the effectiveness of an initial antiviral innate immune response, resulting in the upregulation of interferon (IFN) and, subsequently, IFN-stimulated genes (ISGs). ISGs serve to mount an antiviral state within a host cell, and although the specific antiviral function of a number of ISGs has been characterized, the function of many of these ISGs remains to be determined. Recent research has uncovered a novel role for a handful of ISGs, some of them directly induced by IFN regulatory factor 3 in the absence of IFN itself. These ISGs, most with potent antiviral activity, are also able to augment varying arms of the innate immune response to viral infection, thereby strengthening this response. This new understanding of the role of ISGs may, in turn, help the recent advancement of novel therapeutics aiming to augment innate signaling pathways in an attempt to control viral infection and pathogenesis.

scholarly journals Antigen Microarrays for the Study of Autoimmune Diseases

2013 ◽  
Vol 59 (7) ◽  
pp. 1036-1044 ◽  
Author(s):  
Ada Yeste ◽  
Francisco J Quintana
Keyword(s):  
Immune Response ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Disease Diagnosis ◽  
Autoimmune Disorders ◽  
Response To Therapy ◽  
Autoimmune Response ◽  
Molecular Pathways ◽  
Systemic Lupus

BACKGROUND The immune response involves the activation of heterogeneous populations of T cells and B cells that show different degrees of affinity and specificity for target antigens. Although several techniques have been developed to study the molecular pathways that control immunity, there is a need for high-throughput assays to monitor the specificity of the immune response. CONTENT Antigen microarrays provide a new tool to study the immune response. We reviewed the literature on antigen microarrays and their advantages and limitations, and we evaluated their use for the study of autoimmune diseases. Antigen arrays have been successfully used for several purposes in the investigation of autoimmune disorders: for disease diagnosis, to monitor disease progression and response to therapy, to discover mechanisms of pathogenesis, and to tailor antigen-specific therapies to the autoimmune response of individual patients. In this review we discuss the use of antigen microarrays for the study of 4 common autoimmune diseases and their animal models: type 1 diabetes, systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis. CONCLUSIONS Antigen microarrays constitute a new tool for the investigation of the immune response in autoimmune disorders and also in other conditions such as tumors and allergies. Once current limitations are overcome, antigen microarrays have the potential to revolutionize the investigation and management of autoimmune diseases.

Plasmacytoid Dendritic Cells (PDC) and Th17 Immune Response Contribution in Gut Acute Graft-Versus-Host-Disease (GVHD)

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2968-2968
Author(s):  
Florent Malard ◽  
Céline Bossard ◽  
Jessy Arbez ◽  
Patrice Chevallier ◽  
Thierry Guillaume ◽  
...  
Keyword(s):  
Immune Response ◽  
Stem Cell ◽  
Autoimmune Diseases ◽  
Intestinal Mucosa ◽  
Th17 Cells ◽  
Acute Gvhd ◽  
Type I ◽  
Type I Ifn ◽  
Th17 Response

Abstract Abstract 2968 Background. Acute GVHD after allogeneic stem cell transplantation (allo-SCT) is an exaggerated immune response against alloantigens involving dysregulation of inflammatory cytokine cascades. Previous studies established an important role of Th1 cells in acute GVHD pathophysiology. However, the identification of proinflammatory Th17 cells which contribute to autoimmune diseases pathophysiology, raised the issue of the role of Th17 cells in human acute GVHD. Indeed, the contribution of Th17 cells in acute GVHD was assessed in GVHD mouse models with conflicting results. In addition, the role of the PDC subset (the professional type I IFN-secreting cells), which play an important role in triggering Th17-related cytokines and autoimmune diseases, is not yet established in the acute GVHD setting. This report investigated the role of Th17 cells and their interaction with PDC in gastrointestinal (GI) biopsies taken from patients with or without acute GVHD. Patients and Methods. Studies described in this report were performed in a single centre series of 21 patients who underwent allo-SCT for different hematological malignancies (n=19) and severe aplastic anemia (n=2). The median age of patients was 53 years (range, 16–69). The stem cell source was PBSCs in 19 cases (85%), CB in 2 cases and BM in one case. Ten patients received transplant from a matched-related donor, and 11 patients from a matched-unrelated donor. A reduced-intensity conditioning regimen was used in the majority of cases (n=19; 90%) Immunohistochemistry was performed on deparaffinized tissues sections using an indirect immunoperoxydase method. A quantitative evaluation of antigens expression was performed by counting the number of positive cells in the whole biopsy at 200 magnifications for each sample. Results. In this cohort, based on standard pathology criteria, 16 patients had a histologically proven gastrointestinal acute GVHD. In all cases, biopsies were taken before initiation of systemic corticosteroid therapy. The remaining 5 patients did not have histological signs of acute GVHD (and did not develop clinical signs of acute GVHD) and thus, were used as controls. In order to identify the Th17 cell population, biopsies were tested for expression of the CD161 and CCR6 markers, and ROR-gamma-t, the key transcription factor that orchestrates the differentiation of Th17 cells. Significantly higher numbers of ROR-gamma-t+ and CD161+ cells were counted in the intestinal mucosa of patients with acute GVHD compared with intestinal mucosa of patients without acute GVHD, mainly found in the lamina propria but also in the epithelium of altered glands (p=0.016 and p=0.009 for ROR-gamma-t and CD161 expression respectively). Given the role of PDCs in triggering Th17-related cytokines, we sought next to determine the proportion of PDCs in intestinal biopsies from these same patients. This analysis showed a significant increase of CD123+ PDCs in the intestinal mucosa of patients with acute GVHD compared with mucosa of patients without acute GVHD (p=0.017). Moreover, we observed a significant correlation between the number of CD123+ PDCs and ROR-gamma-t or CD161 expressing cells in the intestinal mucosa of acute GVHD patients, highlighting the link between PDC and Th17 cells. Conclusion. The current study shed some light on the role of Th17 cells in the context of gastro-intestinal acute GVHD. Using well-established specific markers, we show that Th17 cells infiltrate intestinal biopsies from patients with acute GVHD. In addition, Th17 infiltration was paralleled by the infiltration of PDCs, suggesting a potential new pathophysiological link between PDCs and Th17 response in the context of gastro-intestinal acute GVHD. This is consistent with studies showing that PDCs can drive the differentiation of Th17 cells. Functional analyses are currently ongoing. Although the exact mechanism that links type I IFN production to PDC-mediated Th17 responses is still unclear in acute GVHD, these data raise the prospect of future innovative approaches to optimize immunosuppression regimens for the treatment or prophylaxis of acute GVHD by targeting PDCs and the Th17 response. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Depletion of Neutrophils Exacerbates the Early Inflammatory Immune Response in Lungs of Mice Infected withParacoccidioides brasiliensis

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Paula Andrea Pino-Tamayo ◽  
Juan David Puerta-Arias ◽  
Damaris Lopera ◽  
Martha Eugenia Urán-Jiménez ◽  
Ángel González
Keyword(s):  
Monoclonal Antibody ◽  
Immune Response ◽  
Inflammatory Response ◽  
Paracoccidioides Brasiliensis ◽  
Yeast Cells ◽  
Histopathological Analysis ◽  
Acute Inflammatory Response ◽  
Fungal Load ◽  
Inflammatory Immune Response

Neutrophils predominate during the acute phase of theParacoccidioides brasiliensisinfection. Herein, we determined the role of the neutrophil during the early stages of experimental pulmonary paracoccidioidomycosis using a monoclonal antibody (mAb) specific for neutrophils. Male BALB/c mice were inoculated intranasally with1.5×106or2×106P. brasiliensisyeast cells. The mAb was administered 24 h before infection, followed by doses every 48 h until mice were sacrificed. Survival time was evaluated and mice were sacrificed at 48 h and 96 h after inoculation to assess cellularity, fungal load, cytokine/chemokine levels, and histopathological analysis. Neutrophils from mAb-treated mice were efficiently depleted (99.04%). Eighty percent of the mice treated with the mAb and infected with1.5×106yeast cells died during the first two weeks after infection. When mice were treated and infected with2×106yeast cells, 100% of them succumbed by the first week after infection. During the acute inflammatory response significant increases in numbers of eosinophils, fungal load and levels of proinflammatory cytokines/chemokines were observed in the mAb-treated mice. We also confirmed that neutrophils are an important source of IFN-γand IL-17. These results indicate that neutrophils are essential for protection as well as being important for regulating the early inflammatory immune response in experimental pulmonary paracoccidioidomycosis.

scholarly journals The Role of IL-36 in the Pathophysiological Processes of Autoimmune Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Wen-jian Chen ◽  
Xiao Yu ◽  
Xin-Rong Yuan ◽  
Bang-jie Chen ◽  
Na Cai ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Inflammatory Response ◽  
Autoimmune Diseases ◽  
Future Research ◽  
Dependent Manner ◽  
Receptor Complexes ◽  
Multiple Organs ◽  
Pro Inflammatory Cytokines

A member of the interleukin (IL)-1 superfamily was IL-36, which contained IL-36α, IL-36β, IL-36γ, and IL-36Ra. Heterotrimer complexes, consisting of heterodimeric receptor complexes and IL-36 agonist, gave signals through intracellular functional domains, so as to bind to downstream proteins and induce inflammatory response. IL-36 agonists upregulated mature-associated CD80, CD86, MHCII, and inductively produced several pro-inflammatory cytokines through the IL-36R-dependent manner in dendritic cells (DCs). Besides, DCs had the ability to initiate the differentiation of helper T (Th) cells. Up to date, the role of IL-36 in immunity, inflammation and other diseases is of great importance. Additionally, autoimmune diseases were characterized by excessive immune response, resulting in damage and dysfunction of specific or multiple organs and tissues. Most autoimmune diseases were related to inflammatory response. In this review, we will conclude the recent research advances of IL-36 in the occurrence and development of autoimmune diseases, which may provide new insight for the future research and the treatment of these diseases.

Plasmacytoid Dendritic Cells (PDC) and Th17 Immune Response Contribution in Skin Acute Graft-Versus-Host-Disease (GVHD)

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4103-4103
Author(s):  
Florent Malard ◽  
Céline Bossard ◽  
Patrice Chevallier ◽  
Thierry Guillaume ◽  
Jacques Delaunay ◽  
...  
Keyword(s):  
Immune Response ◽  
Stem Cell ◽  
Autoimmune Diseases ◽  
Th17 Cells ◽  
Acute Gvhd ◽  
Unrelated Donor ◽  
Type I ◽  
Type I Ifn ◽  
Th17 Response

Abstract Abstract 4103 Background. Acute GVHD after allogeneic stem cell transplantation (allo-SCT) is an exaggerated immune response against alloantigens involving dysregulation of inflammatory cytokine cascades. Previous studies established an important role of Th1 cells in acute GVHD pathophysiology. However, the identification of proinflammatory Th17 cells which contribute to autoimmune diseases pathophysiology, raised the issue of the role of Th17 cells in human acute GVHD. Indeed, the contribution of Th17 cells in acute GVHD was assessed in GVHD mouse models with conflicting results. In addition, the role of the PDC subset (the professional type I IFN-secreting cells), which play an important role in triggering Th17-related cytokines and autoimmune diseases, is not yet established in the acute GVHD setting. This report investigated the role of Th17 cells and their interaction with PDC in cutaneous biopsies taken from patients with or without acute GVHD. Patients and Methods. Studies described in this report were performed in a single centre series of 38 patients who underwent allo-SCT for different hematological malignancies (n=37) and severe aplastic anemia (n=1). The median age of patients was 52 years (range, 17–70). The stem cell source was PBSCs in 27 cases (71%), CB in 6 cases and BM in 5 cases. 11 patients received transplant from a matched-related donor, and 27 patients from an unrelated donor. A reduced-intensity conditioning regimen was used in the majority of cases (n=29; 76%) Immunohistochemistry was performed on deparaffinized tissues sections using an indirect immunoperoxydase method. A quantitative evaluation of antigens expression was performed by counting the number of positive cells in the whole biopsy at 200 magnifications for each sample. Results. In this cohort, based on standard pathology criteria, 29 patients had a histologically proven skin acute GVHD. In all cases, biopsies were taken before initiation of systemic corticosteroid therapy. The remaining 9 patients did not have histological signs of acute GVHD (and did not develop clinical signs of acute GVHD) and thus, were used as controls. In order to identify the Th17 cell population, biopsies were tested for expression of the CD161 and CCR6 markers, and ROR-gamma-t, the key transcription factor that orchestrates the differentiation of Th17 cells. Significantly higher numbers of ROR-gamma-t+, CD161+ and CCR6+ cells were counted in the skin of patients with acute GVHD compared with intestinal mucosa of patients without acute GVHD, mainly found in the lamina propria but also in the epithelium of altered glands (p=0.001, p<0.0001 and p=0.01 for ROR-gamma-t, CD161 and CCR6 expression respectively).Given the role of PDCs in triggering Th17-related cytokines, we sought next to determine the proportion of PDCs in cutaneous biopsies from these same patients. This analysis showed a significant increase of BDCA2+ PDCs in the skin of patients with acute GVHD compared with skin of patients without acute GVHD (p=0.03). Moreover, we observed a strong expression of the type I IFN-inducible protein Mx1 in the skin of patients with acute GVHD compared with skin of patients without acute GVHD, reflecting the high production of type I IFN by the BDCA2+ PDCs. Conclusion. The current study shed some light on the role of Th17 cells in the context of cutaneous acute GVHD. Using well-established specific markers, we show that Th17 cells infiltrate skin biopsies from patients with acute GVHD. In addition, Th17 infiltration was paralleled by the infiltration of PDCs, suggesting a potential new pathophysiological link between PDCs and Th17 response in the context of cutaneous acute GVHD. This is consistent with studies showing that PDCs can drive the differentiation of Th17 cells. Functional analyses are currently ongoing. These data raise the prospect of future innovative approaches to optimize immunosuppression regimens for the treatment or prophylaxis of acute GVHD by targeting PDCs and the Th17 response. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Recent Advances in Unveiling the Role of Beta-Herpesviruses in Autoimmune Diseases

2021 ◽  
Vol 9 (12) ◽  
pp. 2572
Author(s):  
Maria Cristina Arcangeletti ◽  
Elisabetta Caselli
Keyword(s):  
Immune Response ◽  
Autoimmune Diseases ◽  
Immune Tolerance ◽  
Normal Cells ◽  
Recent Advances ◽  
Self Antigens

A dysregulated immune response can lead to recognition of self-antigens as non-self-antigens, leading to failure of the immune tolerance toward normal cells and tissues, and the consequent development of a variety of autoimmune diseases [...]

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