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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
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Stimulation of neutrophil apoptosis by immobilized IgA

Jorge Schettini1, Gabriela Salamone, Analía Trevani

  • 1Laboratory of Immunology, Institute of Hematologic Research, National Academy of Medicine, and Laboratory of Immunogenetics, Department of Microbiology, Buenos Aires University School of Medicine, Argentina.

Journal of Leukocyte Biology
|October 16, 2002
PubMed

Insights

Immobilized immunoglobulin A (IgA) significantly increases neutrophil apoptosis, a process dependent on CD18/CD11b interactions and respiratory burst activation. This finding may inform understanding of autoimmune diseases like IgA nephropathy.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Neutrophil apoptosis is crucial for resolving inflammation.
  • Immunoglobulin A (IgA) plays a role in mucosal immunity and immune complex diseases.
  • The specific mechanisms by which IgA influences neutrophil lifespan are not fully understood.

Purpose of the Study:

  • To investigate the effect of different forms of immunoglobulin A (IgA) on neutrophil apoptosis.
  • To elucidate the molecular pathways involved in IgA-mediated modulation of neutrophil apoptosis.

Main Methods:

  • Neutrophils were cultured with immobilized plasma IgA (iIgAp), immobilized secretory IgA (iIgAs), soluble IgA, or aggregated IgA.
  • Blocking antibodies against CD18 or CD11b were used to assess the role of integrins.
  • Catalase and azide were employed to evaluate the involvement of the respiratory burst.
  • Neutrophils from chronic granulomatous disease patients were used to confirm the role of the respiratory burst.

Main Results:

  • Immobilized IgA (iIgAp and iIgAs) significantly increased neutrophil apoptosis rates.
  • Soluble or aggregated IgA had no effect on neutrophil apoptosis.
  • The pro-apoptotic effect of immobilized IgA was inhibited by blocking antibodies to CD18/CD11b.
  • Apoptosis promotion by immobilized IgA was dependent on respiratory burst activation, as evidenced by catalase inhibition and azide potentiation.
  • Immobilized IgA did not induce apoptosis in neutrophils from chronic granulomatous disease patients.

Conclusions:

  • Immobilized IgA, but not soluble or aggregated forms, promotes neutrophil apoptosis.
  • This process involves CD18/CD11b integrins and is dependent on the activation of the respiratory burst.
  • IgA-induced neutrophil apoptosis may play a role in regulating inflammation in autoimmune conditions like IgA nephropathy.

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