Lymphotoxin detected in the blister fluid of bullous pemphigoid patients.

Edward W B Jeffes,Gale A Granger,Robert S Yamamoto,A Razzaque Ahmed

doi:10.1007/bf00915284

Edward W B Jeffes, Gale A Granger + Show 2 more

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https://doi.org/10.1007/bf00915284

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Abstract

The role of lymphocytes in the pathogenesis of bullous pemphigoid was examined by assaying the blister fluid obtained from bullous pemphigoid patients for the presence of the lymphokine, lymphotoxin. Blister fluids from six bullous pemphigoid were assayed on L-929 target cells for the presence of cytolytic molecules in the standard lymphotoxin assay. Three of six blister fluids obtained from bullous pemphigoid patients and one linear IgA bullous dermatosis patient contained significant levels of cytolytic activity. Control blister fluids from suction blisters, herpes, pemphigus, and toxic epidermal necrolysis patients did not contain cytolytic activity. Serum from five bullous pemphigoid patients also had no cytolytic activity. Neutralization studies using rabbit anti-alpha-lymphotoxin demonstrated that 54 to 88% of the cytolytic activity found in bullous pemphigoid blister fluid was due to alpha-lymphotoxin. These results indicate that lymphotoxin is locally released in the skin of bullous pemphigoid lesions and is detectable in blister fluids.

Highlights

The events initiating and regulating the disease processes causing bullous pemphigoid (BP) are not well understood
Blister fluid from six BP patients and one linear IgA bullous dermatosis patient were assayed on L929 in the standard lymphotoxin assay system as described in Materials and Methods
Control blister fluid from suction blisters raised in three volunteers, two pemphigus vulgaris patients, one toxic epidermal necrolysis patient, and one herpes zoster patient did not contain cytolytic activity

Summary

Introduction

The events initiating and regulating the disease processes causing bullous pemphigoid (BP) are not well understood. IgG and complement are found in BP lesions, they alone do not explain the pathogenesis of this disease (t, 2). Morphological studies of the bullous lesions seen late in the. UCLA School of Medicine, Los Angeles, California 90024, and Department of Molecular Biology and Biochemistry, University of California at lrvine, trvine. :To whom correspondence should be addressed at Division of Dermatology, UCLA School of Medicine, Los Angeles.

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