PMID- 31448653
OWN - NLM
STAT- MEDLINE
DCOM- 20200819
LR  - 20200819
IS  - 1549-781X (Electronic)
IS  - 1040-8363 (Linking)
VI  - 56
IP  - 8
DP  - 2019 Dec
TI  - Post-translational modifications of proteins in antiphospholipid antibody 
      syndrome.
PG  - 511-525
LID - 10.1080/10408363.2019.1650714 [doi]
AB  - Antiphospholipid antibody syndrome (APS) is a systemic autoimmune disease 
      characterized by arterial and venous thrombosis and/or pregnancy morbidity. The 
      incidence is around five new cases/100,000 persons per year and the prevalence is 
      around 40-50 cases/100,000. The prevalence is higher (about 30%) among patients 
      with systemic lupus erythematosus. APS is associated with circulating 
      antiphospholipid antibodies (aPLs), a heterogeneous group of autoantibodies 
      directed against negatively charged molecules and a combination of 
      protein-complexed phospholipids. The predominant protein antigen in this disorder 
      is beta 2-glycoprotein I (beta2GPI). Despite the discovery of "new" antigenic 
      targets and development of "new" methodological approaches, the laboratory 
      diagnosis of APS is still an evolving field and studies to identify further 
      antigenic target(s) as potential diagnostic markers and risk predictors are in 
      progress. In particular, recent studies were aimed at analyzing the pathogenic 
      role of post-translational modifications (PTMs) of proteins induced by 
      inflammation and/or oxidative stress as modulators of protein structure and 
      function and possibly as a source of antigenic epitopes. The present review is 
      focused on PTMs of self-proteins responsible for autoimmune reactions in patients 
      with APS. At present, the known PTMs in APS involve beta2GPI. In particular, the PTM 
      of beta2GPI via thiol-exchange reactions is a highly specific phenomenon that makes 
      the protein more antigenic. Other PTMs, including sialylation and acetylation, 
      may affect beta2GPI antigenicity. Moreover, the addition or loss of carbohydrate 
      chains affects beta2GPI immunoreactivity since carbohydrates are determining factors 
      for beta2GPI conformation. In addition to beta2GPI, PTMs of other self proteins such as 
      vimentin and annexins may play a role in the immune response during APS. The 
      study of PTMs is useful to clarify the role of modified proteins in the 
      pathogenesis of APS as well as to design more efficient diagnostic/prognostic 
      tools and more targeted therapeutic approaches.
FAU - Buttari, Brigitta
AU  - Buttari B
AD  - Department of Cardiovascular and Endocrine-Metabolic Diseases and Aging, Istituto 
      Superiore di Sanita , Rome , Italy.
FAU - Profumo, Elisabetta
AU  - Profumo E
AD  - Department of Cardiovascular and Endocrine-Metabolic Diseases and Aging, Istituto 
      Superiore di Sanita , Rome , Italy.
FAU - Capozzi, Antonella
AU  - Capozzi A
AD  - Department of Experimental Medicine, Sapienza University of Rome , Rome , Italy.
FAU - Saso, Luciano
AU  - Saso L
AUID- ORCID: 0000-0003-4530-8706
AD  - Department of Physiology and Pharmacology, "Vittorio Erspamer", Sapienza 
      University of Rome , Rome , Italy.
FAU - Sorice, Maurizio
AU  - Sorice M
AD  - Department of Experimental Medicine, Sapienza University of Rome , Rome , Italy.
FAU - Rigano, Rachele
AU  - Rigano R
AD  - Department of Cardiovascular and Endocrine-Metabolic Diseases and Aging, Istituto 
      Superiore di Sanita , Rome , Italy.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20190826
PL  - England
TA  - Crit Rev Clin Lab Sci
JT  - Critical reviews in clinical laboratory sciences
JID - 8914816
RN  - 0 (Autoantigens)
RN  - 0 (Proteins)
SB  - IM
MH  - Antiphospholipid Syndrome/*metabolism
MH  - Autoantigens/immunology
MH  - Autoimmunity
MH  - Humans
MH  - Oxidative Stress
MH  - *Protein Processing, Post-Translational
MH  - Proteins/*metabolism
OTO - NOTNLM
OT  - Antiphospholipid antibody syndrome
OT  - inflammation
OT  - oxidative stress
OT  - post-translational modification
OT  - beta2-glycoprotein I
EDAT- 2019/08/27 06:00
MHDA- 2020/08/20 06:00
CRDT- 2019/08/27 06:00
PHST- 2019/08/27 06:00 [pubmed]
PHST- 2020/08/20 06:00 [medline]
PHST- 2019/08/27 06:00 [entrez]
AID - 10.1080/10408363.2019.1650714 [doi]
PST - ppublish
SO  - Crit Rev Clin Lab Sci. 2019 Dec;56(8):511-525. doi: 
      10.1080/10408363.2019.1650714. Epub 2019 Aug 26.