p53-dependent senescence delays EI1 4-myc-induced B-cell lymphomagenesis
There are 2 comments on the Nature Publishing Group story from Nov 23, 2009, titled p53-dependent senescence delays EI1 4-myc-induced B-cell lymphomagenesis. In it, Nature Publishing Group reports that:
E-mail: [email protected] Received 6 May 2009; Revised 17 August 2009; Accepted 25 September 2009; Published online 23 November 2009.
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#1 Feb 27, 2010
HIV corrupting nearby cells such as whose job it is to detect damaged self cells,ie p53 may become activated by a self antigen-presenting B cell.
Such a damage detecting cell is, for example, known as an effector T cell (Teff) example; a gamma delta T cell, also referred to as a γδT cell (γδ refers to the chains of its receptor). protein p51 p53 & p55
The γδT cell can then seek out other sites of inflammation (for example in the brain in MS, Alzheimers and in the heart for auto-immune myocarditis, in the pancreas in the case of Type I Diabetes). Alternatively, the γδT cell might attempt to kill the CD4+ T cell that may respond to self antigens.
These discoveries have important implications in the treatment of infectious disease. For example, HIV disease is characterized by rapidly dividing, activated B cells that cause enlargement of the lymph nodes in the HIV infected individuals. It has been discovered herein that the B cells from an HIV infected lymph node have high levels of CLIP, indicating that the B cells have been non-specifically activated. In fact, the lymph node is filled with B cells intertwined with infected CD4 T cells. It has been discovered that replacement of the CLIP on the surface of the B cell with a target peptide having high affinity for the specific MHC of that individual, would result in activation of the Treg cells. As described in more detail below, a group of thymus derived peptides can function as these specific target peptides.
Also computational methods can be used to predict additional target peptides, as shown according to the invention. It has recently been shown that there is a strong correlation between the presence of Tregs and the length of time of infection prior to full-blown AIDS. Moreover, as Treg numbers decline, there is a concomitant rise in viral load in that individual. Thus, the invention involves the discovery that replacement of CLIP on the MHC with specific peptides described herein as well as custom-designed and computationally predicted “targeted peptides” could reactivate Tregs and dampen the pathological inflammation that is required for an increase in virally infected cells.
Appropriate targeted peptides can be synthesized based on patient specific MHC information in order to treat HIV positive individuals with all different types of MHC fingerprints. mhc, B 25 crossover ions are affected an cause the main dysfuction in long term B memory cells! which lead to non activation of CD 4 cells thus no HIV immune response;
#2 Feb 27, 2010
AIDS kills a lot of knee-grows
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