PMID- 14961984
OWN - NLM
STAT- MEDLINE
DCOM- 20041007
LR  - 20230124
IS  - 1600-6135 (Print)
IS  - 1600-6135 (Linking)
VI  - 4
IP  - 3
DP  - 2004 Mar
TI  - Non-complement- and complement-activating antibodies synergize to cause rejection 
      of cardiac allografts.
PG  - 326-34
AB  - Alloantibodies (AlloAbs) are a clinically significant component of the immune 
      response to organ transplants. In our experimental model, B10.A (H-2a) cardiac 
      transplants survived significantly longer in C57BL/6 (H-2b) immunoglobulin 
      knock-out (IgKO) recipients than in their wild-type (WT) counterparts. Passive 
      transfer of a single 50-200-microg dose of complement-activating IgG2b AlloAbs to 
      IgKO recipients reconstituted acute rejection of cardiac allografts. Although 
      passive transfer of a subthreshold dose of 25 microg of IgG2b or a single 
      100-200-microg dose of non-complement-activating IgG1 AlloAbs did not restore 
      acute rejection to IgKO recipients, a combination of these AlloAbs did cause 
      acute graft rejection. Histologically, rejection was accompanied by augmented 
      release of von Willebrand factor from endothelial cells. IgG1 AlloAbs did not 
      activate complement on their own and did not augment complement activation by 
      IgG2b AlloAbs. However, IgG1 AlloAbs stimulated cultured mouse endothelial cells 
      to produce monocyte chemotactic protein 1 (MCP-1) and neutrophil chemoattractant 
      growth-related oncogene alpha (KC). TNF-alpha augmented IgG1 induced secretion of 
      MCP-1 and KC. These findings indicate that non-complement-activating AlloAbs can 
      augment injury to allografts by complement-activating AlloAbs. 
      Non-complement-activating AlloAbs stimulate endothelial cells to produce 
      chemokines and this effect is augmented in the milieu of proinflammatory 
      cytokines.
FAU - Rahimi, Salma
AU  - Rahimi S
AD  - Department of Pathology, The Johns Hopkins University School of Medicine, 
      Baltimore, MD, USA.
FAU - Qian, Zhiping
AU  - Qian Z
FAU - Layton, Jodi
AU  - Layton J
FAU - Fox-Talbot, Karen
AU  - Fox-Talbot K
FAU - Baldwin, William M 3rd
AU  - Baldwin WM 3rd
FAU - Wasowska, Barbara A
AU  - Wasowska BA
LA  - eng
GR  - P01 HL 56091/HL/NHLBI NIH HHS/United States
GR  - R01 HL 63948/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Transplant
JT  - American journal of transplantation : official journal of the American Society of 
      Transplantation and the American Society of Transplant Surgeons
JID - 100968638
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Isoantibodies)
RN  - 9007-36-7 (Complement System Proteins)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/immunology/pharmacology
MH  - Complement System Proteins/*immunology
MH  - Drug Synergism
MH  - Graft Rejection/chemically induced/*immunology
MH  - Heart Transplantation/*immunology
MH  - Immunoglobulin G/immunology/pharmacology
MH  - Isoantibodies/immunology
MH  - Mice
EDAT- 2004/02/14 05:00
MHDA- 2004/10/08 09:00
CRDT- 2004/02/14 05:00
PHST- 2004/02/14 05:00 [pubmed]
PHST- 2004/10/08 09:00 [medline]
PHST- 2004/02/14 05:00 [entrez]
AID - S1600-6135(22)07462-7 [pii]
AID - 10.1111/j.1600-6143.2004.00334.x [doi]
PST - ppublish
SO  - Am J Transplant. 2004 Mar;4(3):326-34. doi: 10.1111/j.1600-6143.2004.00334.x.