PMID- 12515286
OWN - NLM
STAT- MEDLINE
DCOM- 20030502
LR  - 20190922
IS  - 0891-6934 (Print)
IS  - 0891-6934 (Linking)
VI  - 35
IP  - 5
DP  - 2002 Aug
TI  - Detection of cytotoxic anti-LEDGF autoantibodies in atopic dermatitis.
PG  - 319-27
AB  - In the last two decades, atopic dermatitis (AD) has been of increasing clinical 
      significance in Japan. Eight-20% of patients with AD developed progressive 
      cataracts (cataract-AD) and lens epithelial cells (LECs) were severely damaged. 
      Lens epithelium-derived growth factor (LEDGF) is a newly isolated survival 
      factor. In the presence of LEDGF, LECs survive well and in the absence of LEDGF, 
      they become highly susceptible to stress. We investigated (1) whether 
      auto-antibody (auto-Ab) to LEDGF is present in sera of AD patients and (2) 
      whether depletion of LEDGF by the auto-Ab kills LECs. In sera from 26 patients 
      with AD using ELISA, we found significantly higher levels of auto-Ab to LEDGF 
      than that in a normal control group. Affinity purified auto-Ab to LEDGF from 
      these sera killed LECs without complement activation. Levels of histamine in the 
      AD group were significantly higher and levels of prostaglandin E2 were 
      significantly lower than in the normal group. However, statistically there are no 
      differences between sera from AD and cataract-AD in levels of Ab to LEDGF, 
      histamine, prostaglandin E2 (PGE2), immunoglobulin E (IgE) and eosinophiles. We 
      speculate that cataract-AD may be induced, in part, by a combination of high 
      levels of serum histamine and eye rubbing which could break the blood-aqueous 
      barrier to allow the entry of Ab to LEDGF into the privileged compartment, thus, 
      reducing LEDGF levels, resulting in damage to LECs, and cataract formation.
FAU - Ayaki, Masahiko
AU  - Ayaki M
AD  - Center for Ophthalmic Research, Brigham and Women's Hospital, Department of 
      Ophthalmology, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, 
      USA.
FAU - Ohoguro, Nobuyuki
AU  - Ohoguro N
FAU - Azuma, Noriyuki
AU  - Azuma N
FAU - Majima, Yoshinao
AU  - Majima Y
FAU - Yata, Kiyomi
AU  - Yata K
FAU - Ibaraki, Nobuhiro
AU  - Ibaraki N
FAU - Singh, Dhirendra P
AU  - Singh DP
FAU - Ko, Vincent
AU  - Ko V
FAU - Shinohara, Toshimichi
AU  - Shinohara T
LA  - eng
GR  - EY10958/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Autoimmunity
JT  - Autoimmunity
JID - 8900070
RN  - 0 (Autoantibodies)
RN  - 0 (Immunoglobulins)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (lens epithelium-derived growth factor)
RN  - 820484N8I3 (Histamine)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Autoantibodies/*blood
MH  - Case-Control Studies
MH  - Cataract/blood/complications/immunology
MH  - Cytotoxicity, Immunologic
MH  - Dermatitis, Atopic/blood/complications/*immunology
MH  - Dinoprostone/blood
MH  - Eosinophils
MH  - Epithelial Cells/immunology
MH  - Histamine/blood
MH  - Humans
MH  - Immunoglobulins/blood
MH  - In Vitro Techniques
MH  - Intercellular Signaling Peptides and Proteins/*immunology
MH  - Lens, Crystalline/immunology
MH  - Mice
EDAT- 2003/01/08 04:00
MHDA- 2003/05/03 05:00
CRDT- 2003/01/08 04:00
PHST- 2003/01/08 04:00 [pubmed]
PHST- 2003/05/03 05:00 [medline]
PHST- 2003/01/08 04:00 [entrez]
AID - 10.1080/0891693021000003198 [doi]
PST - ppublish
SO  - Autoimmunity. 2002 Aug;35(5):319-27. doi: 10.1080/0891693021000003198.