Abstract:
:Transferrin receptor (TfR) expression is up-regulated during T cell activation after the interaction of the T cell receptor with the antigen-major histocompatibility complex and the expression of interleukin-2 (IL-2) receptor. We hypothesize that anti-TfR monoclonal antibody (mAb) will prolong allograft survival by altering T cell responses. In a murine heterotopic nonvascularized cardiac allograft model, CBA/J (H-2k) recipients were transplanted with neonatal C57BL/6 (H-2b) donor hearts. Anti-TfR or isotype-matched control mAbs (100 microg) were administered at the time of transplantation and on the following day. Splenocytes from naive CBA/J mice were stimulated in vitro with C57BL/6 alloantigen. Anti-TfR mAb was administered at 5 microg/mL during the initiation of culture. Cytotoxic T lymphocyte (CTL) and mixed lymphocyte responses (MLR) were performed to assess T cell function. After 24 h in culture, cells were harvested, RNA isolated, and semi-quantitative reverse transcriptase-polymerase chain reaction performed. Anti-TfR mAb prolonged allograft survival to 25.7 +/- 0.9 days compared to the isotype control (10.7 +/- 0.4 days, P < 0.01, Wilcoxon rank sum). Anti-TfR mAb completely abrogated the CTL response and suppressed the MLR by 70-86% compared to the isotype controls. Anti-TfR mAb suppressed IL-2, interferon-gamma (IFN-gamma), IL-10, and IL-12 p40 mRNA expression, but had no effect on IL-4, IL-12 p35, and IL-15 mRNA expression. In conclusion, anti-TfR mAb prolongs allograft survival, suppresses T cell function, and alters IL-2, IL-10, IL-12 p40, and IFN-gamma mRNA expression. These data suggest that the down-regulation in IL-12 mRNA by anti-TfR mAb may prevent the development of T helper cells, thereby promoting graft survival and altering cell-mediated immune responses. The partial effect by anti-TfR mAb on cytokine mRNA expression may be due to other contributing factors such as costimulation.
journal_name
J Leukoc Bioljournal_title
Journal of leukocyte biologyauthors
Bayer AL,Baliga P,Woodward JEdoi
10.1002/jlb.64.1.19subject
Has Abstractpub_date
1998-07-01 00:00:00pages
19-24issue
1eissn
0741-5400issn
1938-3673journal_volume
64pub_type
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journal_title:Journal of leukocyte biology
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pub_type: 杂志文章
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journal_title:Journal of leukocyte biology
pub_type: 杂志文章
doi:
更新日期:2002-05-01 00:00:00
abstract::Chemokines regulate the migration and the maturation of dendritic cells (DC) licensed by microbial constituents. We have recently found that the function of DC, including their ability to activate naïve, allogeneic CD4+ T cells, requires the autocrine/paracrine release of the nuclear protein high mobility group box 1 ...
journal_title:Journal of leukocyte biology
pub_type: 杂志文章
doi:10.1189/jlb.0306171
更新日期:2007-01-01 00:00:00
abstract::Sexual transmission is the primary route of HIV-1 infection, and DC subsets are thought to be involved in viral dissemination to T cells. In the genital mucosa, two main subsets of DCs are present: epithelial LCs capture and degrade HIV-1 through C-type lectin Langerin, whereas subepithelial DCs express DC-SIGN, which...
journal_title:Journal of leukocyte biology
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journal_title:Journal of leukocyte biology
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更新日期:2014-11-01 00:00:00
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journal_title:Journal of leukocyte biology
pub_type: 杂志文章,评审
doi:10.1189/jlb.0409230
更新日期:2009-09-01 00:00:00
abstract::Apoptotic loss of CD4+ T cells has been proposed as a mechanism of T cell depletion in human immunodeficiency virus (HIV) infections resulting in immunodeficiency. The Env glycoprotein has been implicated in apoptosis of uninfected bystander cells via gp120 binding to CD4/CXC chemokine receptor 4 as well as the fusion...
journal_title:Journal of leukocyte biology
pub_type: 杂志文章
doi:10.1189/jlb.0805430
更新日期:2006-02-01 00:00:00
abstract::Mer signaling participates in a novel inhibitory pathway in TLR activation. The purpose of the present study was to examine the role of Mer signaling in the down-regulation of TLR4 activation-driven immune responses in mice, i.t.-treated with LPS, using the specific Mer-blocking antibody. At 4 h and 24 h after LPS tre...
journal_title:Journal of leukocyte biology
pub_type: 杂志文章
doi:10.1189/jlb.0611289
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journal_title:Journal of leukocyte biology
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journal_title:Journal of leukocyte biology
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journal_title:Journal of leukocyte biology
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journal_title:Journal of leukocyte biology
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更新日期:1992-10-01 00:00:00
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journal_title:Journal of leukocyte biology
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journal_title:Journal of leukocyte biology
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journal_title:Journal of leukocyte biology
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journal_title:Journal of leukocyte biology
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journal_title:Journal of leukocyte biology
pub_type: 杂志文章
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