Immunology

Apoptosis and Autoimmunity: From Mechanisms to Treatments by Joachim R. Kalden, Martin Herrmann

By Joachim R. Kalden, Martin Herrmann

This is often the 1st accomplished publication in regards to the courting among apoptosis and autoimmune illnesses. It deals a different up to date evaluate on learn effects at the faulty execution of apoptosis and the unfinished clearance of apoptotic cells. The molecular and mobile mechanisms concerned are defined intimately. As a potential end result of apoptotic disorder, the improvement of serious autoimmune ailments (e.g., rheumatoid arthritis, systemic lupus erythematosus) is mentioned. An outlook on destiny study themes contains the assessment of novel healing techniques.

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Additional resources for Apoptosis and Autoimmunity: From Mechanisms to Treatments

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Zheng, T. , Rakic, P. and Flavell, R A. Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice. Nature 1996, 384, 368–72. , Soengas, M. , Duncan, G. , Kaufman, S. , Lowe, S. W. and Mak, T. W. Essential contribution of caspase-3/CPP32 to apoptosis and its associated nuclear changes. Genes Dev 1998, 12, 806–19. , Braun, M. , Denis, F. and Sekaly, R. P. Specific activation of the cysteine protease CPP32 during the negative selection of T cells in the thymus. J Exp Med 1997, 186, 1503–12.

The route leading from ER stress to caspase-12 activation, however, remains unclear. There is evidence, however, suggesting that release of intracellular calcium stores associated with ER stress activates the protease calpain, which in turn can activate caspase-12 and lead to apoptosis [105]. 10 Compensatory Caspase Activation: A Caveat to Knockout Analysis Although the generation of knockout animals has vastly increased our knowledge of the cellular apoptotic machinery, one difficulty in assessing the contributions of individual proteins has been the ability to preserve function by the compensatory activation of related proteins.

And Wallach, D. Targeted disruption of the mouse Caspase-8 gene ablates cell death induction by the TNF receptors, Fas/Apo1, and DR3 and is lethal prenatally. Immunity 1998, 9, 267–76. , Surh, C. D. and Sprent, J. 1998, A role for Fas in negative selection of thymocytes in vivo. J Exp Med 187, 1427–38. Sidman, C. , Marshall, J. D. and Von Boehmer, H. Transgenic T cell receptor interactions in the lymphoproliferative and autoimmune syndromes of lpr and gld mutant mice. Eur J Immunol 1992, 22, 499–504.

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