A New Approach of Abnormal Apoptosis Implicated in Malignancy and Autoimmunity
- *Corresponding Author:
- Aurelian Udristioiu
Emergency County Hospital Targu Jiu
Clinical Laboratory, Gorj, Romania
Tel: +40 (723) 621 414
Fax: +40 (253) 210 218
E-mail: [email protected]
Received Date: October 21, 2011; Accepted Date: April 18, 2012; Published Date: April 21, 2012
Citation: Udristioiu A, Iliescu R, Udristioiu L, Cojocaru M (2012) A New Approach of Abnormal Apoptosis Implicated in Malignancy and Autoimmunity. J Bioanal Biomed 4:034-038. doi:10.4172/1948-593X.1000061
Copyright: © 2012 Udristioiu A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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 selfreactive 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 and micro RNAs (miRNAs).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.