PMID- 22903673
OWN - NLM
STAT- MEDLINE
DCOM- 20121001
LR  - 20171116
IS  - 0065-2598 (Print)
IS  - 0065-2598 (Linking)
VI  - 750
DP  - 2012
TI  - Granulocyte death regulation by naturally occurring autoantibodies.
PG  - 157-72
LID - 10.1007/978-1-4614-3461-0_12 [doi]
AB  - 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.
FAU - von Gunten, Stephan
AU  - von Gunten S
AD  - Institute of Pharmacology, University of Bern, Switzerland. 
      stephan.vongunten@pki.unibe.ch
FAU - Simon, Hans-Uwe
AU  - Simon HU
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Adv Exp Med Biol
JT  - Advances in experimental medicine and biology
JID - 0121103
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation, B-Lymphocyte)
RN  - 0 (Autoantibodies)
RN  - 0 (FAS protein, human)
RN  - 0 (Lectins)
RN  - 0 (SIGLEC8 protein, human)
RN  - 0 (SIGLEC9 protein, human)
RN  - 0 (Sialic Acid Binding Immunoglobulin-like Lectins)
RN  - 0 (fas Receptor)
SB  - IM
MH  - Antigens, CD/immunology/metabolism
MH  - Antigens, Differentiation, B-Lymphocyte/immunology/metabolism
MH  - Apoptosis/*immunology
MH  - Autoantibodies/*immunology/metabolism
MH  - Cell Count
MH  - Granulocytes/*immunology/metabolism/pathology
MH  - Humans
MH  - Immunity, Innate
MH  - Inflammation/immunology/metabolism/pathology
MH  - Lectins/immunology/metabolism
MH  - Sialic Acid Binding Immunoglobulin-like Lectins
MH  - Signal Transduction/*immunology
MH  - fas Receptor/immunology/metabolism
EDAT- 2012/08/21 06:00
MHDA- 2012/10/02 06:00
CRDT- 2012/08/21 06:00
PHST- 2012/08/21 06:00 [entrez]
PHST- 2012/08/21 06:00 [pubmed]
PHST- 2012/10/02 06:00 [medline]
AID - 10.1007/978-1-4614-3461-0_12 [doi]
PST - ppublish
SO  - Adv Exp Med Biol. 2012;750:157-72. doi: 10.1007/978-1-4614-3461-0_12.