PMID- 14724434
OWN - NLM
STAT- MEDLINE
DCOM- 20040219
LR  - 20171116
IS  - 0041-1337 (Print)
IS  - 0041-1337 (Linking)
VI  - 77
IP  - 1
DP  - 2004 Jan 15
TI  - The role of B7 ligands (CD80 and CD86) in CD152-mediated allograft tolerance: a 
      crosscheck hypothesis.
PG  - 48-54
AB  - BACKGROUND: The regulatory mechanism by which the B7 ligands (CD80 and CD86) 
      direct the CD28/CD152 costimulatory pathways is unclear. This study investigated 
      the role of CD80 and CD86 in a CD152-mediated allograft tolerance model. METHODS: 
      A low-responding cardiac transplant model (BALB/c-->B10.A) with possible 
      long-term acceptance was used. Immunocytochemical and flow cytometric analyses of 
      the graft-infiltrating cells were conducted to characterize this transplant 
      model. The influence of anti-CD80 and anti-CD86 treatments on the proliferation 
      and interleukin (IL)-2 productions of the tolerated splenocytes (SC) was 
      analyzed. The role of CD80 and CD86 in the induction and maintenance of the graft 
      acceptance in this transplant model were also tested. RESULTS: B10.A mice could 
      accept the BALA/c cardiac allografts (11/22), and an anti-CD152 antibody blocked 
      the graft acceptance (10/10). Immunocytochemical and flow cytometric analyses 
      showed that CD152+ cells were predominant among the CD4+ cells infiltrating the 
      100-day grafts of the B10.A recipients (B10.A-100). Either anti-CD80 or anti-CD86 
      treatment significantly enhanced polyclonal proliferation and IL-2 production of 
      the B10.A-100 SC. Blockade of either CD80 or CD86 prohibited the tolerance 
      transmitted by adoptive transfer, and anti-CD80 or anti-CD86 plus skin grafting 
      undermined the established allograft tolerance. CONCLUSIONS: Both CD80 and CD86 
      were essential for the induction and maintenance of the CD152-mediated allograft 
      tolerance.
FAU - Tsai, Meng-Kun
AU  - Tsai MK
AD  - Department of Surgery, National Taiwan University Hospital and National Taiwan 
      University College of Medicine, Taipei, Taiwan.
FAU - Ho, Hong-Nerng
AU  - Ho HN
FAU - Chien, Hsiung-Fei
AU  - Chien HF
FAU - Ou-Yang, Pu
AU  - Ou-Yang P
FAU - Lee, Chun-Jean
AU  - Lee CJ
FAU - Lee, Po-Huang
AU  - Lee PH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Transplantation
JT  - Transplantation
JID - 0132144
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation)
RN  - 0 (B7-1 Antigen)
RN  - 0 (B7-2 Antigen)
RN  - 0 (CD4 Antigens)
RN  - 0 (CTLA-4 Antigen)
RN  - 0 (Cd86 protein, mouse)
RN  - 0 (Ctla4 protein, mouse)
RN  - 0 (Interleukin-2)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Receptors, Interleukin-2)
RN  - 11028-71-0 (Concanavalin A)
SB  - IM
MH  - Adoptive Transfer
MH  - Animals
MH  - Antigens, CD/*immunology/pharmacology
MH  - Antigens, Differentiation/metabolism
MH  - B7-1 Antigen/immunology/*metabolism
MH  - B7-2 Antigen
MH  - CD4 Antigens/metabolism
MH  - CTLA-4 Antigen
MH  - Cell Division
MH  - Concanavalin A/pharmacology
MH  - Female
MH  - Graft Survival
MH  - Heart Transplantation/*immunology
MH  - Interleukin-2/biosynthesis
MH  - Membrane Glycoproteins/*immunology/pharmacology
MH  - Mice
MH  - Mice, Inbred Strains
MH  - *Models, Immunological
MH  - Monocytes/metabolism/pathology
MH  - Myocardium/metabolism/pathology
MH  - Receptors, Interleukin-2/metabolism
MH  - Spleen/drug effects/metabolism/pathology
MH  - Time Factors
MH  - *Transplantation Tolerance/drug effects
MH  - Transplantation, Homologous
EDAT- 2004/01/16 05:00
MHDA- 2004/02/20 05:00
CRDT- 2004/01/16 05:00
PHST- 2004/01/16 05:00 [pubmed]
PHST- 2004/02/20 05:00 [medline]
PHST- 2004/01/16 05:00 [entrez]
AID - 10.1097/01.TP.0000107286.21985.EF [doi]
PST - ppublish
SO  - Transplantation. 2004 Jan 15;77(1):48-54. doi: 10.1097/01.TP.0000107286.21985.EF.