scholarly journals Ancestry-based differences in the immune system are associated with lupus severity

2021 ◽  
Author(s):  
Samantha Slight-Webb ◽  
Kevin Thomas ◽  
Miles Smith ◽  
Susan Macwana ◽  
Aleksandra Bylinska ◽  
...  
Keyword(s):  
Immune Cells ◽  
Lupus Erythematosus ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Mass Cytometry ◽  
Microbial Infection ◽  
Younger Age ◽  
Soluble Mediator ◽  
Immune Alterations ◽  
Key Drivers

Abstract Systemic lupus erythematosus (SLE) affects 1 in 537 of African American (AA) women, which is >2-fold more than European American (EA) women. AA patients also develop the disease at a younger age, have more severe symptoms, and a greater chance of early mortality. We used a multi-omics approach to uncover ancestry-specific immune alterations in SLE patients and healthy controls that may contribute to disease disparities. Cell composition, signaling, and epigenetics were evaluated by mass cytometry; droplet-based single cell transcriptomics and paired proteogenomics (scRNA-Seq/scCITE-Seq). Soluble mediator levels were measured in plasma and stimulated whole blood. Toll-like receptor (TLRs) pathways are activated by vaccination and microbial infection, and are also key drivers of autoimmune disease. We observed enhanced TLR3/4/7/8/9-related gene expression in immune cells from AA versus EA SLE patients. TLR7/8/9 and IFNα phospho-signaling responses were heightened even in immune cells from healthy AA versus EA controls. TLR stimulation of healthy AA and EA immune cells recapitulated the distinct ancestry-associated SLE immunophenotypes. Thus, healthy individuals show ancestry-based differences in innate immune pathways that could influence the course and severity of lupus and other diseases.

Role of Inflammasome Activation in Systemic Lupus Erythematosus: Are Innate Immune Cells Activated?

2020 ◽  
Author(s):  
Rodolfo Perez-Alamino ◽  
Raquel Cuchacovich ◽  
Luis R. Espinoza ◽  
Constance P. Porretta ◽  
Arnold H. Zea
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune Cells ◽  
Lupus Erythematosus ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Innate Immune Cells ◽  
Systemic Lupus

scholarly journals Serum vitamin D/25(OH)D associated with toll-like receptor (TLR) 2 expression of immune cells in the saliva of Systemic Lupus Erythematosus: a preliminary study

2021 ◽  
Vol 27 (2) ◽  
pp. 22
Author(s):  
Hendri Susanto ◽  
Bagus Soebadi ◽  
Diah Savitri Ernawati ◽  
Adiastuti Endah Pamardiati ◽  
Hening Tuti Hendarti ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Vitamin D ◽  
Immune Cells ◽  
Lupus Erythematosus ◽  
Serum Vitamin ◽  
Toll Like Receptor ◽  
Systemic Lupus ◽  
Tlr2 Expression ◽  
Cross Sectional ◽  
Serum Vitamin D

Objective: Vitamin D deficiency may contribute to Systemic Lupus Erythematosus (SLE) development. Vitamin D may involve in pathogen recognition through Toll-like receptor (TLR) 2 in immune cells in saliva. This study aimed to determine the correlation between serum vitamin D/25(OH)D and TLR2 expression of immune cells in the saliva of SLE. Materials and methods: This cross-sectional study conducted at the the SLE patients who met the inclusion and exclusion criteria. Those who had signed informed consent involved to underwent unstimulated saliva collection and blood samples for TLR2 and vitamin D/25(OH)D examination. The correlation between serum vitamin D/25(OH)D concentration and salivary TLR2 expression was analyzed using the correlation test, linear regression with 95% confidence level. Results: Thirty SLE patients had a mean serum vitamin D/25(OH)D concentration of 9.98 ± 4.64 ng/ml. The mean of TLR2 expression of CD11b+ cells in saliva was 26.03 ± 20.92%. There was a significant positive correlation between serum vitamin D/25(OH)D concentration and TLR 2 expression of CD11b+ cells in the saliva. (r = 0.434; P < 0.05). Vitamin D/25(OH)D was the only predictor for TLR 2 expression. Conclusion: Serum vitamin D/25(OH)D concentrations associated with TLR2 expression of CD11b+ cells in the saliva of SLE.

scholarly journals Toll-Like Receptor 8 Agonist and Bacteria Trigger Potent Activation of Innate Immune Cells in Human Liver

2014 ◽  
Vol 10 (6) ◽  
pp. e1004210 ◽  
Author(s):  
Juandy Jo ◽  
Anthony T. Tan ◽  
James E. Ussher ◽  
Elena Sandalova ◽  
Xin-Zi Tang ◽  
...  
Keyword(s):  
Immune Cells ◽  
Human Liver ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Toll Like Receptor

scholarly journals Nonbilayer Phospholipid Arrangements Are Toll-Like Receptor-2/6 and TLR-4 Agonists and Trigger Inflammation in a Mouse Model Resembling Human Lupus

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Carlos Wong-Baeza ◽  
Alonso Tescucano ◽  
Horacio Astudillo ◽  
Albany Reséndiz ◽  
Carla Landa ◽  
...  
Keyword(s):  
B Cells ◽  
Lupus Erythematosus ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Autoantibody Production ◽  
Immune System Activation ◽  
Expression Of Genes ◽  
Nuclear Antigens ◽  
Proinflammatory Gene ◽  
Toll Like Receptor 2

Systemic lupus erythematosus is characterized by dysregulated activation of T and B cells and autoantibodies to nuclear antigens and, in some cases, lipid antigens. Liposomes with nonbilayer phospholipid arrangements induce a disease resembling human lupus in mice, including IgM and IgG antibodies against nonbilayer phospholipid arrangements. As the effect of these liposomes on the innate immune response is unknown and innate immune system activation is necessary for efficient antibody formation, we evaluated the effect of these liposomes on Toll-like receptor (TLR) signaling, cytokine production, proinflammatory gene expression, and T, NKT, dendritic, and B cells. Liposomes induce TLR-4- and, to a lesser extent, TLR-2/TLR-6-dependent signaling in TLR-expressing human embryonic kidney (HEK) cells and bone marrow-derived macrophages. Mice with the lupus-like disease had increased serum concentrations of proinflammatory cytokines, C3a and C5a; they also had more TLR-4-expressing splenocytes, a higher expression of genes associated with TRIF-dependent TLR-4-signaling and complement activation, and a lower expression of apoptosis-related genes, compared to healthy mice. The percentage of NKT and the percentage and activation of dendritic and B2 cells were also increased. Thus, TLR-4 and TLR-2/TLR-6 activation by nonbilayer phospholipid arrangements triggers an inflammatory response that could contribute to autoantibody production and the generation of a lupus-like disease in mice.

scholarly journals Innate Immune Cells and Toll-like Receptor–Dependent Responses at the Maternal–Fetal Interface

2019 ◽  
Vol 20 (15) ◽  
pp. 3654 ◽  
Author(s):  
Andrea Olmos-Ortiz ◽  
Pilar Flores-Espinosa ◽  
Ismael Mancilla-Herrera ◽  
Rodrigo Vega-Sánchez ◽  
Lorenza Díaz ◽  
...  
Keyword(s):  
Immune Cells ◽  
Expression Profiles ◽  
Cell Types ◽  
Innate Immune ◽  
Toll Like Receptor ◽  
Decidual Cells ◽  
Hofbauer Cells ◽  
Peptide Expression ◽  
Antimicrobial Peptide Expression ◽  
Maternal Fetal Interface

During pregnancy, the placenta, the mother and the fetus exploit several mechanisms in order to avoid fetal rejection and to maintain an immunotolerant environment throughout nine months. During this time, immune cells from the fetal and maternal compartments interact to provide an adequate defense in case of an infection and to promote a tolerogenic milieu for the fetus to develop peacefully. Trophoblasts and decidual cells, together with resident natural killer cells, dendritic cells, Hofbauer cells and other macrophages, among other cell types, contribute to the modulation of the uterine environment to sustain a successful pregnancy. In this review, the authors outlined some of the various roles that the innate immune system plays at the maternal–fetal interface. First, the cell populations that are recruited into gestational tissues and their immune mechanisms were examined. In the second part, the Toll–like receptor (TLR)–dependent immune responses at the maternal–fetal interface was summarized, in terms of their specific cytokine/chemokine/antimicrobial peptide expression profiles throughout pregnancy.

scholarly journals Flagellin A Toll-Like Receptor 5 Agonist as an Adjuvant in Chicken Vaccines

2014 ◽  
Vol 21 (3) ◽  
pp. 261-270 ◽  
Author(s):  
Shishir Kumar Gupta ◽  
Preety Bajwa ◽  
Rajib Deb ◽  
Madhan Mohan Chellappa ◽  
Sohini Dey
Keyword(s):  
Infectious Diseases ◽  
Immune Cells ◽  
Cytokine Production ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Vaccine Adjuvants ◽  
Toll Like Receptor ◽  
Absolute Requirement ◽  
Toll Like Receptor 5 ◽  
Potential Use

ABSTRACTChicken raised under commercial conditions are vulnerable to environmental exposure to a number of pathogens. Therefore, regular vaccination of the flock is an absolute requirement to prevent the occurrence of infectious diseases. To combat infectious diseases, vaccines require inclusion of effective adjuvants that promote enhanced protection and do not cause any undesired adverse reaction when administered to birds along with the vaccine. With this perspective in mind, there is an increased need for effective better vaccine adjuvants. Efforts are being made to enhance vaccine efficacy by the use of suitable adjuvants, particularly Toll-like receptor (TLR)-based adjuvants. TLRs are among the types of pattern recognition receptors (PRRs) that recognize conserved pathogen molecules. A number of studies have documented the effectiveness of flagellin as an adjuvant as well as its ability to promote cytokine production by a range of innate immune cells. This minireview summarizes our current understanding of flagellin action, its role in inducing cytokine response in chicken cells, and the potential use of flagellin as well as its combination with other TLR ligands as an adjuvant in chicken vaccines.

scholarly journals Ageing and Toll-like receptor expression by innate immune cells in chronic human schistosomiasis

2007 ◽  
Vol 149 (2) ◽  
pp. 274-284 ◽  
Author(s):  
F. Comin ◽  
E. Speziali ◽  
O. A. Martins-Filho ◽  
I. R. Caldas ◽  
V. Moura ◽  
...  
Keyword(s):  
Immune Cells ◽  
Innate Immune ◽  
Receptor Expression ◽  
Innate Immune Cells ◽  
Toll Like Receptor ◽  
Human Schistosomiasis
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