PMID- 22041579
OWN - NLM
STAT- MEDLINE
DCOM- 20120927
LR  - 20211020
IS  - 1873-0183 (Electronic)
IS  - 1568-9972 (Linking)
VI  - 11
IP  - 8
DP  - 2012 Jun
TI  - Autoantibodies in lupus: culprits or passive bystanders?
PG  - 596-603
LID - 10.1016/j.autrev.2011.10.021 [doi]
AB  - Several autoantibodies are culprits in the pathogenesis of organ damage in 
      systemic lupus erythematosus, by means of established or postulated mechanisms, 
      whereby inducing a perturbation of cell structure and function, with consequent 
      tissue-organ impairment. Common autoantibody-mediated mechanisms of damage 
      include cell surface binding with or without cytolysis, immune complex-mediated 
      damage, penetration into living cells, binding to cross-reactive extracellular 
      molecules. Experimental data from both murine models and humans have recently 
      clarified the key role of autoantibodies in severe organ involvements, including 
      nephritis, neuropsychiatric (NP) dysfunction, and cerebrovascular disease (CVD). 
      In lupus nephritis early and late phases are distinguishable and mediated by 
      different processes in which anti-chromatin antibodies are both inducing and 
      perpetuating agents, by immune-complex formation and massive deposition in 
      mesangial matrix at first, and in glomerular basement membrane at end-stage. Also 
      NP abnormalities occur very early, much earlier than other systemic 
      manifestations, and exacerbate with the increase in autoantibody titers. Among 
      the autoantibodies mainly implicated in neurolupus, anti-beta2 glycoprotein I 
      (beta2GPI) antibodies are preferentially involved in focal NP events which are a 
      consequence of non-inflammatory microangiopathy; otherwise, anti-ribosomal P 
      protein antibodies and N-methyl-d-aspartate receptor (NMDAR) antibodies cause 
      diffuse NP events through a direct cytotoxic effect on neuronal cells at specific 
      brain zones.
CI  - Copyright (c) 2011 Elsevier B.V. All rights reserved.
FAU - Rekvig, Ole P
AU  - Rekvig OP
AD  - Molecular Pathology Research Group, Institute of Medical Biology, University of 
      Tromso, Norway.
FAU - Putterman, Chaim
AU  - Putterman C
FAU - Casu, Cinzia
AU  - Casu C
FAU - Gao, Hua-Xin
AU  - Gao HX
FAU - Ghirardello, Anna
AU  - Ghirardello A
FAU - Mortensen, Elin S
AU  - Mortensen ES
FAU - Tincani, Angela
AU  - Tincani A
FAU - Doria, Andrea
AU  - Doria A
LA  - eng
GR  - R01 AR048692/AR/NIAMS NIH HHS/United States
GR  - DK90319/DK/NIDDK NIH HHS/United States
GR  - AR48692/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20111025
PL  - Netherlands
TA  - Autoimmun Rev
JT  - Autoimmunity reviews
JID - 101128967
RN  - 0 (Antigen-Antibody Complex)
RN  - 0 (Autoantibodies)
RN  - 0 (Autoantigens)
RN  - 0 (Chromatin)
RN  - 0 (Membrane Transport Proteins)
RN  - 0 (OCA2 protein, human)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
SB  - IM
MH  - Animals
MH  - Antigen-Antibody Complex/*immunology
MH  - Autoantibodies/*immunology
MH  - Autoantigens/immunology
MH  - Bystander Effect
MH  - Chromatin/immunology
MH  - Cytotoxicity, Immunologic
MH  - Disease Models, Animal
MH  - Glomerular Basement Membrane/*immunology
MH  - Humans
MH  - Lupus Nephritis/diagnosis/*immunology
MH  - Lupus Vasculitis, Central Nervous System/diagnosis/*immunology
MH  - Membrane Transport Proteins/immunology
MH  - Neurons/*immunology
MH  - Receptors, N-Methyl-D-Aspartate/immunology
EDAT- 2011/11/02 06:00
MHDA- 2012/09/28 06:00
CRDT- 2011/11/02 06:00
PHST- 2011/11/02 06:00 [entrez]
PHST- 2011/11/02 06:00 [pubmed]
PHST- 2012/09/28 06:00 [medline]
AID - S1568-9972(11)00241-2 [pii]
AID - 10.1016/j.autrev.2011.10.021 [doi]
PST - ppublish
SO  - Autoimmun Rev. 2012 Jun;11(8):596-603. doi: 10.1016/j.autrev.2011.10.021. Epub 
      2011 Oct 25.