Essentials of Pathophysiology: Concepts of Altered States
Essentials of Pathophysiology: Concepts of Altered States
4th Edition
ISBN: 9781451190809
Author: Carol Porth RN MSN PhD
Publisher: LIPPINCOTT WILLIAMS+WILKINS
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Chapter 45, Problem 1RE
Summary Introduction

To determine: The mechanism of antibodies that attack the glycoproteins in the lamina Lucida and their attachment to the hemi desmosomes that can cause blisters.

Introduction: An infectious disease is the one that is caused by pathogenic microbes. These microbes can be bacteria, parasites, viruses or fungi. They are usually harmless but in some conditions that can be lethal. Infectious diseases can be transmitted from one person (infected) to another person (non-infected).

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Bullous pemphigoid is the most common form of the autoimmune disease that causes the formation of blisters which is induced by the autoantibodies that form against the type XVII collagen. It is an autoimmune subepithelial blistering disease that occurs most frequently in older adults and is characterized by presence of cutaneous bullae and erosive mucosal lesions.

The autoantibodies against the hemidesmosome antigen of type XVII collagen is supposed to induce the inflammatory processes that result in dermal-epidermal separation (BP180). The COL17 is a type II transmembrane protein that spans the lamina Lucida. Most patients have autoantibodies binding to an immunodominant region of BP180, which is located extracellularly close to transmembrane domain of the protein.

Patients’ autoantibodies to BP180 induce dermal-epidermal separation in cryosections of human skin when co-incubated with leukocytes. The loss of cell-matrix adhesion is mediated by proteinases released by granulocytes.

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