Granulocyte death regulation by naturally occurring autoantibodies

von Gunten, Stephan; Simon, Hans-Uwe (2012). Granulocyte death regulation by naturally occurring autoantibodies. Advances in experimental medicine and biology, 750, pp. 157-172. Wien: Springer

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Programmed cell death (PCD) plays a central role in the regulation of granulocytes that are key effector cells of the innate immune system. Granulocytes are produced in high amounts in the bone marrow. A safe elimination of granulocytes by cell death (apoptosis) is essential to maintain the numbers of these cells balanced. In many acute and chronic inflammatory diseases, delayed apoptosis is one mechanism that contributes to accumulation of neutrophil and eosinophil granulocytes at the site of inflammation. On the other hand, a safe elimination of granulocytes by cell death is required to avoid unwanted tissue damage for instance by secretion of toxic products from these cells. Recent evidence shows that humans produce an array of naturally occurring autoantibodies (NAbs) with the capacity to regulate granulocyte death, including agonistic and antagonistic NAbs that bind to the receptors Fas, Siglec-8, and Siglec-9. Together with other factors, these various NAbs exhibit different properties in terms of the form of cell death they induce, the molecular signaling pathways they engage, as well as the efficacy or potency by which they induce cell death. Moreover, several regulatory mechanisms seem to exist that control their biological activity. Novel insights support the concept of granulocyte death regulation by NAbs, which might have important implications for our understanding of the pathogenesis and treatment of inflammatory diseases, including many autoimmune and allergic disorders.

Item Type:

Journal Article (Further Contribution)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology

UniBE Contributor:

von Gunten, Stephan and Simon, Hans-Uwe

ISSN:

0065-2598

Publisher:

Springer

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:35

Last Modified:

08 Jun 2016 10:31

PubMed ID:

22903673

Web of Science ID:

000311931400013

URI:

https://boris.unibe.ch/id/eprint/14093 (FactScience: 220900)

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