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Intracellular antigens released from Balb/c mice kidneys under chemically induced apoptosis and/or necrosis

R Ramírez-Sandoval1, M Vazquez-del-Mercado, A Daneri-Navarro

  • 1Department of Immunology, CBE, Universidad Autonoma de Zacatecas, Mexico.

Reumatismo
|July 25, 2008
PubMed

Insights

Kidney cells undergoing apoptosis and necrosis expose intracellular antigens like Sm, RNP, Ro, and La. This release makes them targets for autoantibodies, potentially contributing to lupus nephritis.

Area of Science:

  • Immunology
  • Pathology
  • Nephrology

Background:

  • Autoimmune diseases like lupus nephritis involve autoantibodies targeting self-antigens.
  • The precise mechanisms of autoantigen exposure in kidney tissue are not fully understood.

Purpose of the Study:

  • To investigate the role of programmed cell death (apoptosis) and necrosis in the exposure of intracellular kidney antigens.
  • To determine if these cellular processes facilitate autoantibody binding in the context of lupus nephritis.

Main Methods:

  • Cultured renal tissues from Balb/c mice were treated with chemical inducers of apoptosis and necrosis.
  • Immunohistochemistry and antibody staining were used to detect the expression of intracellular antigens (Sm, RNP, Ro, La) on the cell surface.

Main Results:

  • Chemical induction of apoptosis and necrosis led to the release and surface exposure of intracellular renal antigens.
  • Exposed antigens, including Sm, RNP, Ro, and La, became accessible for potential autoantibody recognition.

Conclusions:

  • Apoptosis and necrosis are significant mechanisms for exposing intracellular kidney antigens.
  • This antigen exposure may play a crucial role in the pathogenesis of lupus nephritis by making self-antigens targets for autoantibodies.

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