Likewise, it is unclear why in some individuals autoreactive B cell clones become activated and drive pathophysiologic changes in autoimmune diseases.

Broad repertoire autoreactivity may reflect the chances of generating autoreactivity by stochastic use of germline immunoglobulin gene segments or active mechanisms may select autoreactive cells during egress to the naïve peripheral B cell pool. Despite efforts of central tolerance to eliminate these cells, many escape to periphery, where in healthy individuals, they are rendered functionally non-responsive to restimulation through their antigen receptor via a process termed anergy. Most B cells produced in the bone marrow have some level of autoreactivity.

6Medical/Research Service, US Department of Veterans Affairs Medical Center, Oklahoma City, OK, United States.

5Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, United States.

4Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States.

3Rheumatology Section, Medicine Service, Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, CO, United States.

2Human Immunology and Immunotherapy Initiative (HI3), Department of Immunology, University of Colorado School of Medicine, Aurora, CO, United States.

1Division of Rheumatology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO, United States.

Harley 1,2,3*, Kristen Allison 1,2 and R.

Implications and a potential path towards translation.

Potential explanations for gaps in translation.

Risk gene networks for murine autoimmune type 1 diabetes, lupus, central and peripheral B cell tolerance overlap with risk gene networks for human SLE and autoimmune type 1 diabetes.

Gene networks for murine autoimmune type 1 diabetes, lupus, central and peripheral B cell tolerance overlap.

Even the lousiest models of autoimmune disease would predict success if considered in context.

Beyond polygenic genetic structure: Human autoimmune disease and the omnigenic model.

Genetic structure: The usual structure of human autoimmune diseases is polygenic.

Nosology and classification – Autoimmune T1D and the heterogeneity of SLE.

SLE and T1D: Heritability and epidemiology.

Introduction: B cell development, autoimmunity and autoimmune pathology.

The editor and reviewer's affiliations are the latest provided on their Loop research profiles and may not reflect their situation at the time of review. University of Alabama at Birmingham, United States

Sng vs dmg vs martin robey