PMID- 25539820
OWN - NLM
STAT- MEDLINE
DCOM- 20150414
LR  - 20181202
IS  - 1550-6606 (Electronic)
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 194
IP  - 3
DP  - 2015 Feb 1
TI  - TLR2 modulates antibodies required for intestinal ischemia/reperfusion-induced 
      damage and inflammation.
PG  - 1190-8
LID - 10.4049/jimmunol.1303124 [doi]
AB  - In multiple clinical conditions, including trauma and hemorrhage, reperfusion 
      magnifies ischemic tissue damage. Ischemia induces expression of multiple 
      neoantigens, including lipid alterations that are recognized by the serum 
      protein, beta2-glycoprotein I (beta2-GPI). During reperfusion, binding of beta2-GPI by 
      naturally occurring Abs results in an excessive inflammatory response that may 
      lead to death. As beta2-GPI is critical for intestinal ischemia/reperfusion 
      (IR)-induced tissue damage and TLR2 is one of the proposed receptors for beta2-GPI, 
      we hypothesized that IR-induced intestinal damage and inflammation require TLR2. 
      Using TLR2(-/-) mice, we demonstrate that TLR2 is required for IR-induced mucosal 
      damage, as well as complement activation and proinflammatory cytokine production. 
      In response to IR, TLR2(-/-) mice have increased serum beta2-GPI compared with 
      wild-type mice, but beta2-GPI is not deposited on ischemic intestinal tissue. In 
      addition, TLR2(-/-) mice also did not express other novel Ags, suggesting a 
      sequential response. Unlike other TLRs, TLR2(-/-) mice lacked the appropriate Ab 
      repertoire to induce intestinal IR tissue damage or inflammation. Together, these 
      data suggest that, in addition to the inflammatory response, IR-induced injury 
      requires TLR2 for naturally occurring Ab production.
CI  - Copyright (c) 2015 by The American Association of Immunologists, Inc.
FAU - Pope, Michael R
AU  - Pope MR
AD  - Division of Biology, Kansas State University, Manhattan, KS 66506.
FAU - Fleming, Sherry D
AU  - Fleming SD
AD  - Division of Biology, Kansas State University, Manhattan, KS 66506 
      sdflemin@ksu.edu.
LA  - eng
GR  - R21 AI107005/AI/NIAID NIH HHS/United States
GR  - P20 RR016475/RR/NCRR NIH HHS/United States
GR  - R01 AI061691/AI/NIAID NIH HHS/United States
GR  - RR016475/RR/NCRR NIH HHS/United States
GR  - P20 GM103418/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20141224
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Antibodies)
RN  - 0 (Cytokines)
RN  - 0 (Eicosanoids)
RN  - 0 (Immunoglobulin M)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (beta 2-Glycoprotein I)
RN  - 9007-36-7 (Complement System Proteins)
SB  - IM
MH  - Animals
MH  - Antibodies/blood/*immunology
MH  - Complement System Proteins/immunology
MH  - Cytokines/biosynthesis
MH  - Disease Models, Animal
MH  - Eicosanoids/biosynthesis
MH  - Immunoglobulin M/blood/immunology
MH  - Inflammation/genetics/*immunology/*metabolism/pathology
MH  - Intestinal Mucosa/immunology/*metabolism/pathology
MH  - Intestines/*immunology/pathology
MH  - Mice
MH  - Mice, Knockout
MH  - Reperfusion Injury/genetics/*immunology/*metabolism
MH  - Toll-Like Receptor 2/genetics/*metabolism
MH  - beta 2-Glycoprotein I/immunology/metabolism
PMC - PMC4297697
MID - NIHMS645794
EDAT- 2014/12/30 06:00
MHDA- 2015/04/15 06:00
PMCR- 2016/02/01
CRDT- 2014/12/26 06:00
PHST- 2014/12/26 06:00 [entrez]
PHST- 2014/12/30 06:00 [pubmed]
PHST- 2015/04/15 06:00 [medline]
PHST- 2016/02/01 00:00 [pmc-release]
AID - jimmunol.1303124 [pii]
AID - 10.4049/jimmunol.1303124 [doi]
PST - ppublish
SO  - J Immunol. 2015 Feb 1;194(3):1190-8. doi: 10.4049/jimmunol.1303124. Epub 2014 Dec 
      24.