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Fas apoptotic inhibitory molecule 1 [FAIM1]


B cells from aged mice exhibit reduced apoptosis upon B-cell antigen receptor stimulation and differential ability to up-regulate survival signals.

During ageing, autoimmune disorders and the higher susceptibility to infectious have been associated with alterations in the humoral immune response. We report that splenic B lymphocytes from aged mice exhibit lower level of apoptosis induced by B-cell antigen receptor (BCR) ligation in vitro. Respect to B cells from young mice the anti-mu stimulated aged B cells show similar Bcl-2 and Bcl-xL expression but differential kinetic of A1 degradation and a higher level of cFLIP and FAIM. Even though B cells from aged mice show minor Fas expression they exhibit the same susceptibility to anti-Fas induced apoptosis. Aged B cells also present upon BCR stimulation, a higher proliferative response and similar level of activation markers expression than B cells from young mice. These data agree with the observation that aged mice exhibit an increment of T2 and mature B cell subset which rapidly enters cell cycle upon BCR engagement. The diminished apoptosis after activation in aged mice could compromise homeostatic mechanism allowing the persistence of self and non-self antigen specific B cells.

MeSH Terms

  • Aging
  • Animals
  • Antigens
  • Apoptosis
  • Apoptosis Regulatory Proteins
  • B-Lymphocyte Subsets
  • Biomarkers
  • Blotting, Western
  • CASP8 and FADD-Like Apoptosis Regulating Protein
  • Cell Survival
  • Cells, Cultured
  • Electrophoresis, Polyacrylamide Gel
  • Female
  • Flow Cytometry
  • Inhibitor of Apoptosis Proteins
  • Intracellular Signaling Peptides and Proteins
  • Mice
  • Mice, Inbred BALB C
  • Receptors, Antigen, B-Cell
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction
  • Up-Regulation
  • fas Receptor