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Updated: Jun 28, 2026

Supervised Machine Learning for Semi-Quantification of Extracellular DNA in Glomerulonephritis

Supervised Machine Learning for Semi-Quantification of Extracellular DNA in Glomerulonephritis

Published on: June 18, 2020

Disease patterns in vasculitis-still a mystery.

Gary S Hoffman¹

¹Department of Rheumatic and Immmunologic Diseases, Cleveland Clinic Lerner College of Medicine, Cleveland, OH 44195, USA. hoffmag@ccf.org

Bulletin of the NYU Hospital for Joint Diseases

|October 22, 2008

Summary

Vasculitis may originate from new antigens on blood vessel walls, triggering an immune response. This explains organ-specific patterns in autoimmune vascular diseases.

Area of Science:

Immunology
Vascular Biology
Autoimmunity

Background:

Current understanding of autoimmunity focuses on immune cells, cytokines, and antibodies.
The triggers for immune cell migration to injury sites in vasculitis remain largely unknown.
Existing research highlights significant diversity in organ vasculature from early development.

Purpose of the Study:

To propose a novel hypothesis for the etiology of vasculitis.
To explain the organ-specific targeting observed in vasculitis.
To investigate the role of neoantigens in initiating autoimmune vascular disease.

Main Methods:

Review of existing embryological and immunological data.
Formulation of a testable hypothesis based on vascular development and antigen presentation.

More Related Videos

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

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Supervised Machine Learning for Semi-Quantification of Extracellular DNA in Glomerulonephritis

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Published on: June 18, 2020

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

Analysis of factors influencing vascular wall characteristics over time.

Main Results:

Vascular structures exhibit unique developmental and qualitative differences across organs.
These vascular differences are further modified by aging, comorbidities, and other factors.
A hypothesis is proposed linking neoantigen emergence in vessel walls to vasculitis pathogenesis.

Conclusions:

Vasculitis may be initiated by the development of neoantigens within blood vessel walls.
The immune response to these neoantigens could be a normal reaction to perceived foreign proteins.
This hypothesis offers a potential explanation for organ specificity and disease patterns in vasculitis.