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Intracellular ionic changes induced by bullous pemphigoid IgG subclasses

M Suzuki1, S Harada, K Owaribe

  • 1Department of Dermatology Jichi Medical School, Tochigi, Japan.

Autoimmunity
|January 1, 1996
PubMed
Summary
This summary is machine-generated.

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Bullous pemphigoid (BP) IgG1 antibodies trigger intracellular calcium release in DJM-1 cells, but complement activation by BP IgG1 does not lead to cell lysis. Anti-180 kD BP antigen antibodies

Area of Science:

  • Immunodermatology
  • Cellular Signaling
  • Complement Biology

Background:

  • Bullous pemphigoid (BP) is an autoimmune blistering disease.
  • Understanding the role of BP antibodies and complement activation in cellular responses is crucial.

Purpose of the Study:

  • To investigate if bullous pemphigoid (BP) antibodies induce membrane signal transduction.
  • To determine if complement activation by BP antibodies leads to cell lysis.

Main Methods:

  • Assessed intracellular Ca2+ concentration ([Ca2+]i), intracellular pH, membrane potential, and cell morphology using fluorescence microscopy.
  • Incubated DJM-1 cells (squamous cell carcinoma line) with various BP antibodies (IgG1, IgG2, IgG4) and complement.

Main Results:

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  • Certain IgG1 BP antibodies induced a transient increase in intracellular Ca2+ ([Ca2+]i) in DJM-1 cells.
  • Complement activation by BP IgG1 antibodies did not result in observed endocytosis or cell lysis.
  • Monoclonal antibodies against the 180 kD BP antigen showed varied effects on Ca2+ release.

Conclusions:

  • BP IgG1 antibodies can induce Ca2+ release from intracellular stores.
  • Complement activation by BP IgG1 does not appear to cause cell lysis in this model.
  • The role of anti-180 kD BP antigen antibodies in Ca2+ release requires further investigation.