Maintenance of peripheral tolerance to islet antigens

Hamilton‐Williams, Emma E.; Bergot, Anne‐Sophie; Reeves, Peta; Steptoe, Raymond J.

doi:10.1016/j.jaut.2016.05.009

Cited by 7 publications

(3 citation statements)

References 109 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Exhausted T cells do not produce cytokines such as IFN-γ and IL-2, which are needed for T cell effector function (15,16). In addition to reduced expression of IL-7RA, exhausted T cells show an increased expression of inhibitory receptors such as programmed cell death-1 (PD-1) and lymphocyte activation gene-3 (LAG3) (13,15,17). Increased production of the soluble form of IL-7RA via alternative splicing is associated with increased multiple sclerosis risk (18), suggesting a role for IL-7RA in shared mechanisms of autoimmunity.…”

Section: Funding Pfizer Incmentioning

confidence: 99%

Immunomodulatory activity of humanized anti–IL-7R monoclonal antibody RN168 in subjects with type 1 diabetes

Herold¹,

Bucktrout

Wang

et al. 2019

JCI Insight

View full text Add to dashboard Cite

Section: Funding Pfizer Incmentioning

confidence: 99%

Immunomodulatory activity of humanized anti–IL-7R monoclonal antibody RN168 in subjects with type 1 diabetes

Herold¹,

Bucktrout

Wang

et al. 2019

JCI Insight

View full text Add to dashboard Cite

“…To control these self-reactive T cells, several peripheral mechanisms have reported to limit autoimmunity, namely, clone anergy, peripheral deletion, and Tregs. [ 50 51 ] According to the research, Tregs are supposed to participate in the inactivation of autoreactive cells and are the cornerstone component for maintaining peripheral self-tolerance. [ 52 ]…”

Section: Mmunological C Haracteristicsmentioning

confidence: 99%

Immune Tolerance Therapy

Feng

Chen

Yang

et al. 2018

Chinese Medical Journal

View full text Add to dashboard Cite

Objective:Due to the special anatomical structure and pathophysiological mechanism of the central nervous system (CNS), there is a big difference between the repair of brain injury and other systems of the body. More and more evidence shows that targetedly reducing the autoimmune response of brain tissue without affecting the immune function in other parts of the body will be the best optimized treatment for brain injury.Data Sources:This review was based on data in articles published in PubMed up to June 5, 2017, with the following keywords: “immune tolerance”, “traumatic brain injury”, and “central nervous system”.Study Selection:Original articles and critical reviews on immune tolerance and brain damage were selected for this review. References of the retrieved articles were also screened to search for potentially relevant papers.Results:The CNS is isolated from the immune system through the blood-brain barrier. After brain injury, brain antigens are released into the systemic circulation to induce damaging immune responses. Immune tolerance can effectively reduce the brain edema and neurological inflammatory response after brain injury, which is beneficial to the recovery of neurological function. The clinical application prospect and theoretical research value of the treatment of immune tolerance on traumatic brain injury (TBI) is worth attention.Conclusions:The establishment of immune tolerance mechanism has a high clinical value in the treatment of TBI. It opens up new opportunities for the treatment of brain damage.

show abstract

“…The NOD mouse has thus been effectively used to identify loci linked to autoimmune diabetes susceptibility and to understand how these loci influence immune tolerance (Chen et al 2018;Hamilton-Williams et al 2016). Conversely, linkage analysis of defects in immune tolerance can also identify loci linked to autoimmune susceptibility.…”

Section: Introductionmentioning

confidence: 99%

Evidence of genetic epistasis in autoimmune diabetes susceptibility revealed by mouse congenic sublines

Collin

Dugas

Pelletier³

et al. 2021

Immunogenetics

View full text Add to dashboard Cite

Susceptibility to autoimmune diabetes is a complex genetic trait. Linkage analyses exploiting the NOD mouse, which spontaneously develops autoimmune diabetes, has proved to be a useful tool for the characterization of some of these traits. In a linkage analysis using 3A9 TCR transgenic mice on both B10.BR and NOD.H2 k backgrounds, we previously determined that both the Idd2 and Idd13 loci were linked to the proportion of immunoregulatory CD4 -CD8double negative (DN) T cells. In addition to Idd2 and Idd13, five other loci showed weak linkage to the proportion of DN T cells. Of interest, in an interim analysis, a locus on chromosome 12 is linked to DN T cell proportion in both the spleen and the lymph nodes. To determine the impact of this locus on DN T cells, we generated two congenic sublines, which we named Chr12P and Chr12D for proximal and distal, respectively. While 3A9 TCR:insHEL NOD.H2 k -Chr12D mice were protected from diabetes, 3A9 TCR:insHEL NOD.H2 k -Chr12P showed an increase in diabetes incidence. Yet, the proportion of DN T cells was similar to the parental 3A9 TCR NOD.H2 k strain for both of these congenic sublines. A genome-wide two dimensional LOD score analysis reveals genetic epistasis between chromosome 12 and the Idd13 locus. Altogether, this study identified further complex genetic interactions in defining the proportion of DN T cells, along with evidence of genetic epistasis within a locus on chromosome 12 influencing autoimmune susceptibility.

show abstract

Maintenance of peripheral tolerance to islet antigens

Cited by 7 publications

References 109 publications

Immunomodulatory activity of humanized anti–IL-7R monoclonal antibody RN168 in subjects with type 1 diabetes

Immunomodulatory activity of humanized anti–IL-7R monoclonal antibody RN168 in subjects with type 1 diabetes

Immune Tolerance Therapy

Evidence of genetic epistasis in autoimmune diabetes susceptibility revealed by mouse congenic sublines

Contact Info

Product

Resources

About