TY - JOUR
T1 - The role of B7 ligands (CD80 and CD86) in CD152-mediated allograft tolerance: A crosscheck hypothesis
AU - Tsai, Meng-Kun
AU - Ho, Hong-Nerng
AU - Chien, Hsiung-Fei
AU - Ou-Yang, Pu
AU - Lee, Chun-Jean
AU - Lee, Po-Huang
N1 - 被引用次數：16
Export Date: 16 March 2016
CODEN: TRPLA
通訊地址: Lee, P.-H.; Department of Surgery, National Taiwan University Hospital, Chung-Shan South Road, Taipei, 100, Taiwan; 電子郵件： [email protected]
化學物質/CAS: interleukin 2, 85898-30-2; Antigens, CD; Antigens, CD4; Antigens, CD80; Antigens, CD86; Antigens, Differentiation; Cd86 protein, mouse; Concanavalin A, 11028-71-0; cytotoxic T-lymphocyte antigen 4; Interleukin-2; Membrane Glycoproteins; Receptors, Interleukin-2
參考文獻: Lenschow, D.J., Walunas, T.L., Bluestone, J.A., CD28/B7 system of T cell costimulation (1996) Annu Rev Immunol, 14, p. 233; Salomon, B., Bluestone, J.A., Complexities of CD28/B7: CTLA-4 costimulatory pathways in autoimmunity and transplantation (2001) Annu Rev Immunol, 19, p. 225; Carreno, B.M., Bennett, F., Chau, T.A., CTLA-4 (CD152) can inhibit T cell activation by two different mechanisms depending on its level of cell surface expression (2000) J Immunol, 165, p. 1352; Tivol, E., Borriello, F., Schweitzer, A., Loss of CTLA-4 leads to massive lymphoproliferation and fatal multiorgan destruction, revealing a critical negative regulatory role of CTLA-4 (1995) Immunity, 3, p. 541; Waterhouse, P., Penninger, J., Timms, E., Lymproliferative disorders with early lethality in mice deficient in CTLA-4 (1995) Science, 270, p. 985; Perez, V.L., Van Parijis, L., Biuckians, A., Induction of peripheral T cell tolerance in vivo requires CTLA-4 engagement (1997) Immunity, 6, p. 411; Walunas, T.L., Bluestone, J.A., CTLA-4 regulates tolerance induction and T cell differentiation in vivo (1998) J Immunol, 160, p. 3855; Fecteau, S., Basadonna, G.P., Freitas, A., CTLA-4 up-regulation plays a role in tolerance mediated by CD45 (2001) Nat Immunol, 2, p. 58; Read, S., Malmstrom, V., Powrie, F., Cytotoxic T lymphocyte-associated antigen 4 plays an essential role in the function of CD25+CD4+ regulatory cells that control intestinal inflammation (2000) J Exp Med, 192, p. 295; Takahashi, T., Tagami, T., Yamazaki, S., Immunological self-tolerance maintained by CD25+CD4 + regulatory T cells constitutively expressing cytotoxic T lymphocyte-associated antigen 4 (2000) J Exp Med, 192, p. 303; Bour-Jordan, H., Bluestone, J.A., CD28 function: A balance of costimulatory and regulatory signals (2002) J Clin Immunol, 22, p. 1; Collins, A.V., Brodie, D.W., Gilbert, R.J., The interaction properties of costimulatory molecules revisited (2002) Immunity, 17, p. 201; Egen, J.G., Kuhns, M.S., Allison, J.P., CTLA-4: New insights into its biological function and use in tumor immunotherapy (2002) Nat Immunol, 3, p. 611; Judge, T.A., Wu, Z., Zheng, X.G., The role of CD80, CD86, and CTLA-4 in alloimmune responses and the induction of long-term allograft survival (1999) J Immunol, 162, p. 1947; Chai, J.G., Vendetti, S., Amofah, E., CD152 ligation by CD80 on T cells is required for the induction of unresponsiveness by costimulation-deficient antigen presentation (2000) J Immunol, 165, p. 3037; Chen, Z., A technique of cervical heterotopic heart transplantation in mice (1991) Transplantation, 52, p. 1099; Ho, H.N., Chao, K.H., Chen, C.K., The activation status of T and NK cells in the endometrium throughout menstrual cycle and normal and abnormal early pregnancy (1996) Hum Immunol, 49, p. 130; Sheu, B.C., Lin, R.H., Ho, H.N., Down-regulation of CD25 expression on the surface of activated tumor-infiltrating lymphocytes in human cervical carcinoma (1997) Hum Immunol, 56, p. 39; Russell, P.S., Chase, C.M., Colvin, R.B., Alloantibody- and T cell-mediated immunity in the pathogenesis of transplant arteriosclerosis (1997) Transplantation, 64, p. 1531; Sprent, J., Schaefer, M., Lo, D., Properties of purified T cell subsets. II. In vivo response to class I vs class II H-2 differences (1986) J Exp Med, 165, p. 1296; Qin, S., Cobbold, S.P., Pope, H., "Infectious" transplantation tolerance (1993) Science, 259, p. 974; Cobbold, S., Waldmann, H., Infectious tolerance (1998) Curr Opin Immunol, 10, p. 518; Li, X.C., Strom, T.B., Turka, L.A., T cell death and transplantation tolerance (2001) Immunity, 14, p. 407; Alegre, M.L., Noel, P.J., Eisfelder, B.J., Regulation of surface and intracellular expression of CTLA4 on mouse T cells (1996) J Immunol, 157, p. 4762; Dahlen, E., Hedlund, G., Dawe, K., Low CD86 expression in the nonobese diabetic mouse results in the impairment of both T cell activation and CTLA-4 up-regulation (2000) J Immunol, 164, p. 2444; Greenwald, R.J., Oosterwegel, M.A., Van Der Woude, D., CTLA-4 regulates cell cycle progression during a primary immune response (2002) Eur J Immunol, 32, p. 366; Bachmann, M.F., Kohler, G., Ecabert, B., Cutting edge: Lymphoproliferative disease in the absence of CTLA-4 in not T cell autonomous (1999) J Immunol, 163, p. 1128; Chambers, C.A., Kuhns, M.S., Egen, J.G., CTLA-4-mediated inhibition in regulation of T cell responses: Mechanisms and manipulation in tumor immunotherapy (2001) Annu Rev Immunol, 19, p. 565; Eagar, T.N., Karandikar, N.J., Bluestone, J.A., The role of CTLA-4 in induction and maintenance of peripheral T cell tolerance (2002) Eur J Immunol, 32, p. 972
PY - 2004
Y1 - 2004
N2 - 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.
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.
KW - antigen
KW - B7 antigen
KW - CD86 antigen
KW - cytotoxic T lymphocyte antigen 4
KW - interleukin 2
KW - unclassified drug
KW - allotransplantation
KW - animal cell
KW - animal experiment
KW - animal model
KW - antigen function
KW - article
KW - cell infiltration
KW - cell proliferation
KW - clinical pathway
KW - controlled study
KW - cytokine production
KW - female
KW - flow cytometry
KW - heart transplantation
KW - immunocytochemistry
KW - immunological tolerance
KW - long term care
KW - mouse
KW - nonhuman
KW - priority journal
KW - regulatory mechanism
KW - signal transduction
KW - spleen cell
KW - Adoptive Transfer
KW - Animals
KW - Antigens, CD
KW - Antigens, CD4
KW - Antigens, CD80
KW - Antigens, CD86
KW - Antigens, Differentiation
KW - Cell Division
KW - Concanavalin A
KW - Female
KW - Graft Survival
KW - Heart Transplantation
KW - Interleukin-2
KW - Membrane Glycoproteins
KW - Mice
KW - Mice, Inbred Strains
KW - Models, Immunological
KW - Monocytes
KW - Myocardium
KW - Receptors, Interleukin-2
KW - Spleen
KW - Time Factors
KW - Transplantation Tolerance
KW - Transplantation, Homologous
U2 - 10.1097/01.TP.0000107286.21985.EF
DO - 10.1097/01.TP.0000107286.21985.EF
M3 - Article
SN - 0041-1337
VL - 77
SP - 48
EP - 54
JO - Transplantation
JF - Transplantation
IS - 1
ER -