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

By Joachim R. Kalden, Martin Herrmann

This is often the 1st entire ebook concerning the dating among apoptosis and autoimmune ailments. It bargains a different up to date assessment on study 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 critical autoimmune ailments (e.g., rheumatoid arthritis, systemic lupus erythematosus) is mentioned. An outlook on destiny study issues comprises the overview of novel healing suggestions.

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Mice lacking the tumour necrosis factor receptor 1 are resistant to TNF-mediated toxicity but highly susceptible to infection by Listeria monocytogenes. Nature 1993, 364, 798–802. Erickson, S. , de Sauvage, F. , Sheehan, K. , Schreiber, R. , Goeddel, D. V. and Moore, M. W. Decreased sensitivity to tumour-necrosis factor but normal T cell development in TNF receptor-2-deficient mice. Nature 1994, 372, 560–3. Kabra, N. , Hsing, L. , Zhang, J. and Winoto, A. T cell-specific FADD-deficient mice: FADD is required for early T cell development.

J. and ZunigaPflucker, C. p53 prevents maturation to the CD4+CD8+ stage of thymocyte differentiation in the absence of T cell receptor rearrangement. J Exp Med 1996, 183, 1923–8. Linette, G. , Grusby, M. , Hedrick, S. , Hansen, T. , Glimcher, L. H. and Korsmeyer, S. J. Bcl-2 is upregulated at the CD4+ CD8+ stage during positive selection and promotes thymocyte differentiation at several control points. Immunity 1994, 1, 197–205. , Finnegan, A. and Glant, T. T. Spontaneous thymocyte apoptosis is regulated by a mitochondrion-mediated signaling pathway.

Elegans with defective apoptosis initially revealed loss-of-function mutations of the proteins CED-3 (for cell death abnormal) and CED-4, demonstrating their necessity for apoptosis [6]. Subsequently, the protein CED-9 has been identified as an inhibitor of apoptosis functioning upstream of CED-3 and CED-4. Loss-of-function CED-9 mutations cause embryonic lethality due to excess apoptosis, a phenotype that is reversible by loss-of-function CED-3 or CED-4 mutations [7]. Finally, loss-of-function mutations of the protein EGL-1, which binds to CED-9, also suppress apoptosis [8].

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