Biotechnology and Molecular Biology Reviews

  • Abbreviation: Biotechnol. Mol. Biol. Rev.
  • Language: English
  • ISSN: 1538-2273
  • DOI: 10.5897/BMBR
  • Start Year: 2006
  • Published Articles: 101


A new approach of abnormal apoptosis as a cause of autoimmunity and malignancy

Aurelian Udristioiu¹*, Radu G. Iliescu², Lucian Udristioiu¹ and  Manole Cojocaru³
¹Emergency County Hospital Targu Jiu, Clinical Laboratory, Gorj, Romania. 2Polytechnic Institute of New York University, Brooklyn, New York, 11201, USA. ³ Physiology Department, Faculty of Medicine, Titu Maiorescu University, Bucharest, Romania.
Email: [email protected]

  •  Accepted: 12 October 2011
  •  Published: 30 November 2011


Auto-reactive cells which escape from natural apoptosis represent a continuous threat of potential autoimmune response. Abnormal apoptosis can play a role in negative selection of B and T lymphocytes that escaped the self-reactive nature, and so, apoptosis could represent an additional source of auto-antibody. Increased activity of T cells (CD3+, CD4+, or Th1 helper)) will, at a high serum level, cause a high expression of various types of inflammatory interleukins: IL1-β, IL2. The most important regulatory mechanisms of apoptosis in T and B cells are: death receptor cells, CD 95(Fas), TNF-tumor necrosis, caspases, family Bcl-2 proto-oncogenes, Bax gene, p53 tumor suppressor gene, and NF-κB nuclear factor of transcription. The “decision” to undergo programmed cell death is made only in the presence of extrinsic or intrinsic apoptotic messengers. Extrinsic inductors are ligands – cytokines – that bind to death receptors (DRs) found on the cells’ surface, while intrinsic inductors come from the mitochondria or from the nucleus cells.


Key words: Tumor suppressor gene P53, rheumatoid arthritis, systemic lupus erythematosus, tumor necrosis factor, zeta-chain-associated protein kinase 70.