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Translating data from animal models into methods for preventing human autoimmune diabetes mellitus: caveat emptor and primum non nocere - PubMed
Translating data from animal models into methods for preventing human autoimmune diabetes mellitus: caveat emptor and primum non nocere - PubMed
Type 1 diabetes in humans is a serious autoimmune disorder of children that is still poorly understood, unpreventable, and irreversible. Study of its animal models, notably the NOD mouse and BB rat, has generated a wealth of information concerning genetics and immunopathogenesis, but that informatio …
·pubmed.ncbi.nlm.nih.gov·
Translating data from animal models into methods for preventing human autoimmune diabetes mellitus: caveat emptor and primum non nocere - PubMed
Successful prevention of autoimmune disease by transplantation of adequate number of fully allogeneic hematopoietic stem cells - PubMed
Successful prevention of autoimmune disease by transplantation of adequate number of fully allogeneic hematopoietic stem cells - PubMed
We thus report herein the successful prevention of autoimmune disease by transplantation of a sufficiently large number of purified fully allogeneic HSCs in W/B F1 mice.
·pubmed.ncbi.nlm.nih.gov·
Successful prevention of autoimmune disease by transplantation of adequate number of fully allogeneic hematopoietic stem cells - PubMed
Prevention of autoimmune diabetes by oral administration of syngeneic pancreatic extract to young NOD mice - PubMed
Prevention of autoimmune diabetes by oral administration of syngeneic pancreatic extract to young NOD mice - PubMed
Oral administration of relevant autoantigens is being considered as a realistic approach for the prevention of several autoimmune diseases. In this study we administered, orally, to young female NOD/Ak mice (diabetes incidence, 40%) and NOD/LtJ mice (diabetes incidence, 70%) whole pancreatic extract …
·pubmed.ncbi.nlm.nih.gov·
Prevention of autoimmune diabetes by oral administration of syngeneic pancreatic extract to young NOD mice - PubMed
Effect of the synthetic immunomodulator, linomide, on experimental models of thyroiditis - PubMed
Effect of the synthetic immunomodulator, linomide, on experimental models of thyroiditis - PubMed
The drug Linomide is an immunomodulator showing marked down-regulation of several experimental autoimmune diseases. In this study, its effect on three different experimental models of thyroid disease and on spontaneous infiltration of salivary glands (sialoadenitis), was investigated. Although very …
·pubmed.ncbi.nlm.nih.gov·
Effect of the synthetic immunomodulator, linomide, on experimental models of thyroiditis - PubMed
Tonsillectomy does not prevent a progressive course in IgA nephropathy - PubMed
Health Professionals Recruitment and Exposure Program (HPREP) | Office of New Haven Affairs
The therapeutic potential of toll-like receptor 7 stimulation in Asthma — Oregon Health & Science University
Not Found (404) Diversity, Inclusion, Community Engagement, and Equity (DICE)
Toll-Like Receptor Function | ARUP Laboratories Test Directory
Toll-Like Receptor Function | ARUP Laboratories Test Directory
Assist in diagnosis of innate immunodeficiencies when genetic defects of the innate immune system are suspected in individuals negative for other immunodeficiencies (eg, no detectable abnormality of antibody function, complement activity, neutrophil function, or cell-mediated immunity). This test does not measure the function of toll-like receptor 3 (TLR3). Molecular testing is the preferred method for detection of defects in TLR3.
·ltd.aruplab.com·
Toll-Like Receptor Function | ARUP Laboratories Test Directory
Systemic Toll-Like Receptor Stimulation Suppresses Experimental Allergic Asthma and Autoimmune Diabetes in NOD Mice
Systemic Toll-Like Receptor Stimulation Suppresses Experimental Allergic Asthma and Autoimmune Diabetes in NOD Mice
Background Infections may be associated with exacerbation of allergic and autoimmune diseases. Paradoxically, epidemiological and experimental data have shown that some microorganisms can also prevent these pathologies. This observation is at the origin of the hygiene hypothesis according to which the decline of infections in western countries is at the origin of the increased incidence of both Th1-mediated autoimmune diseases and Th2-mediated allergic diseases over the last decades. We have tested whether Toll-like receptor (TLR) stimulation can recapitulate the protective effect of infectious agents on allergy and autoimmunity. Methods and Findings Here, we performed a systematic study of the disease-modifying effects of a set of natural or synthetic TLR agonists using two experimental models, ovalbumin (OVA)-induced asthma and spontaneous autoimmune diabetes, presenting the same genetic background of the non obese diabetic mouse (NOD) that is highly susceptible to both pathologies. In the same models, we also investigated the effect of probiotics. Additionally, we examined the effect of the genetic invalidation of MyD88 on the development of allergic asthma and spontaneous diabetes. We demonstrate that multiple TLR agonists prevent from both allergy and autoimmunity when administered parenterally. Probiotics which stimulate TLRs also protect from these two diseases. The physiological relevance of these findings is further suggested by the major acceleration of OVA-induced asthma in MyD88 invalidated mice. Our results strongly indicate that the TLR-mediated effects involve immunoregulatory cytokines such as interleukin (IL)-10 and transforming growth factor (TGF)-β and different subsets of regulatory T cells, notably CD4+CD25+FoxP3+ T cells for TLR4 agonists and NKT cells for TLR3 agonists. Conclusions/Significance These observations demonstrate that systemic administration of TLR ligands can suppress both allergic and autoimmune responses. They provide a plausible explanation for the hygiene hypothesis. They also open new therapeutic perspectives for the prevention of these pathologies.
·journals.plos.org·
Systemic Toll-Like Receptor Stimulation Suppresses Experimental Allergic Asthma and Autoimmune Diabetes in NOD Mice
Platelets regulate leucocyte responses to Toll-like receptor stimulation. - Abstract - Europe PMC
A Study of JNJ-68284528, a Chimeric Antigen Receptor T Cell (CAR-T) Therapy Directed Against B-cell Maturation Antigen (BCMA) in Participants With Multiple Myeloma - Full Text View - ClinicalTrials.gov
A Study of JNJ-68284528, a Chimeric Antigen Receptor T Cell (CAR-T) Therapy Directed Against B-cell Maturation Antigen (BCMA) in Participants With Multiple Myeloma - Full Text View - ClinicalTrials.gov
A Study of JNJ-68284528, a Chimeric Antigen Receptor T Cell (CAR-T) Therapy Directed Against B-cell Maturation Antigen (BCMA) in Participants With Multiple Myeloma - Full Text View.
·clinicaltrials.gov·
A Study of JNJ-68284528, a Chimeric Antigen Receptor T Cell (CAR-T) Therapy Directed Against B-cell Maturation Antigen (BCMA) in Participants With Multiple Myeloma - Full Text View - ClinicalTrials.gov
Toll-like receptors activation, signaling, and targeting: an overview | Bulletin of the National Research Centre | Full Text
Toll-like receptors activation, signaling, and targeting: an overview | Bulletin of the National Research Centre | Full Text
Background Toll-like receptors (TLRs) are an important family of receptors that constitute the first line of defense system against microbes. They can recognize both invading pathogens and endogenous danger molecules released from dying cells and damaged tissues and play a key role in linking innate and adaptive immunity. TLRs are widely distributed in both immune and other body cells. The expressions and locations of TLRs are regulated in response to specific molecules derived from pathogens or damaged host cells. The binding of ligands to TLR activates specific intracellular signaling cascades that initiate host defense reactions. Such binding is ligand-dependent and cell type-dependent and leads to production of pro-inflammatory cytokines and type 1 interferon. TLR-dependent signaling pathways are tightly increased during innate immune responses by a variety of negative regulators. Overactivation of TLRs can ultimately lead to disruption of immune homeostasis and thus increase the risk for inflammatory diseases and autoimmune disorders. Antagonists/inhibitors targeting the TLR signaling pathways have emerged as novel therapeutics to treat these diseases. Aim of work The present review summarizes the structure, characterizations, and signaling of TLRs and their regulators, as well as describes the implication of TLRs in many diseases with a brief idea about the inhibitors that target TLR signaling pathways. Conclusion We conclude that TLRs are the main elements of our immune system, and they should be maintained functioning to keep the integrity of innate immunity. Targeting of TLR signaling represents a new challenge for treatment of many diseases.
·bnrc.springeropen.com·
Toll-like receptors activation, signaling, and targeting: an overview | Bulletin of the National Research Centre | Full Text
Toll-like receptor 2/6 stimulation promotes angiogenesis via GM-CSF as a potential strategy for immune defense and tissue regeneration | Blood | American Society of Hematology
Toll-like receptor 2/6 stimulation promotes angiogenesis via GM-CSF as a potential strategy for immune defense and tissue regeneration | Blood | American Society of Hematology
Abstract. Toll-like receptors (TLRs) are known primarily as pathogen recognition receptors of the innate immunity, initiating inflammatory pathways to organize
·ashpublications.org·
Toll-like receptor 2/6 stimulation promotes angiogenesis via GM-CSF as a potential strategy for immune defense and tissue regeneration | Blood | American Society of Hematology
Prevention of autoimmune rheumatic disease: state of the art and future perspectives | Annals of the Rheumatic Diseases
Prevention of autoimmune rheumatic disease: state of the art and future perspectives | Annals of the Rheumatic Diseases
Prevention of disease can in principle be accomplished by identification of environmental and/or lifestyle risk and protective factors followed by public health measures (such as for smoking and lung cancer), or by modification of the individual's reactions to disease-inducing factors (such as in vaccinations against microbes). This review discusses both options based on emerging understanding of aetiologies in inflammatory rheumatic diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The major current opportunity for public health-based prevention lies in avoiding smoking. In RA, recent studies have calculated that, in Sweden (a country characterised by a low frequency of smoking), 20% of all RA cases and 33% of all cases of ACPA-positive RA would not have occurred in a smoke-free society. Smoking is also a major risk factor for SLE but no population attribution is yet available. New avenues for individualised and biology-based prevention are provided by the demonstration that several autoimmune rheumatic diseases are preceded by emergence of subclinical autoimmunity followed by laboratory-based signs of inflammation and finally overt disease. Examples of this process are provided from studies of autoimmunity to citrullinated proteins (in RA), to dsDNA (in SLE in general) and to Ro52 epitopes (in the case of neonatal heart block). The recognition of this sequence of events provides opportunities to intervene specifically and potentially curatively before onset of full-blown disease. Such prevention can be accomplished by modification of inciting antigens (environment), by modification of immunity (more or less specific immunomodulation) or by modification of specific gene functions. In all cases, prevention will be different in different subsets of disease and differ at different time points of disease development. Thus, the road map towards prevention of autoimmune rheumatic diseases includes increased understanding of how genes, environment and immunity interact.
·ard.bmj.com·
Prevention of autoimmune rheumatic disease: state of the art and future perspectives | Annals of the Rheumatic Diseases
Predoctoral Program in Cellular, Molecular, and Quantitative Biology Biological & Biomedical Sciences
Predoctoral Program in Cellular, Molecular, and Quantitative Biology Biological & Biomedical Sciences
The CMQB Training Program (CMQBTP) supports 30 predoctoral students per year from the Departments of Molecular Biophysics & Biochemistry, Genetics, Cell Biology
·web.archive.org·
Predoctoral Program in Cellular, Molecular, and Quantitative Biology Biological & Biomedical Sciences
Toll-like receptor stimulation in cardiomyoctes decreases contractility and initiates an NF-κB dependent inflammatory response | Cardiovascular Research | Oxford Academic
Toll-like receptor stimulation in cardiomyoctes decreases contractility and initiates an NF-κB dependent inflammatory response | Cardiovascular Research | Oxford Academic
Abstract. Objective: The transmembrane receptor family of Toll-like receptors (TLRs) may play a role in initiating early inflammatory and functional responses t
·academic.oup.com·
Toll-like receptor stimulation in cardiomyoctes decreases contractility and initiates an NF-κB dependent inflammatory response | Cardiovascular Research | Oxford Academic
Gaslighting in the Academy: Actually Making Black Lives Matter
NIH Training Program Pharmacology
NIH Training Program Pharmacology
Students that are accepted in to the Predoctoral Pharmacology Training Program (PPTP) will be offered a unique training experience focused in the pharmaceutical sciences. The objectives of the PPTP are to train graduate students for a research career in academia, pharmaceutical and biotechnology industries, or
·web.archive.org·
NIH Training Program Pharmacology
Cultural Tax: The Cost of Being the Only or the Few
Enacting Change through Cultivation of Student Activism and Engagement with Diversity, Equity, and Inclusion
Events | Gladstone Institutes
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