Anti-CD3 epsilon F(ab')2 prevents graft-versus-host disease by selectively depleting donor T cells activated by recipient alloantigens. J Immunol 2001 May 01;166(9):5835-9
Date
04/21/2001Pubmed ID
11313428DOI
10.4049/jimmunol.166.9.5835Scopus ID
2-s2.0-0035324638 (requires institutional sign-in at Scopus site) 32 CitationsAbstract
Transplantation tolerance is facilitated by activation-induced apoptosis of peripheral T cells triggered by specific AG: Abs specific for the nonpolymorphic CD3 component of the TCR complex bind to APCs through Fc-FcR interactions, mimic MHC-peptide, and activate polyclonal T cells. In contrast, F(ab')(2) of anti-CD3epsilon Abs do not activate naive T cells but induce apoptosis of Ag-activated, cycling T cells. Here, we report that treatment with anti-CD3epsilon F(ab')(2) can selectively induce apoptosis of donor T cells that recognize a recipient alloantigen, thereby preventing graft-vs-host disease initiated by a TCR-transgenic T cell population. The selective elimination of Ag-activated T cells by non-FcR-binding anti-CD3epsilon Abs could serve as an ideal strategy to prevent graft-vs-host disease and allograft rejection or to treat autoimmune disorders.
Author List
Yu XZ, Bidwell SJ, Martin PJ, Anasetti CAuthor
Xue-Zhong Yu MD Professor in the Microbiology and Immunology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAntibodies, Monoclonal
Antibody-Dependent Cell Cytotoxicity
Apoptosis
CD3 Complex
Cells, Cultured
Cytokines
Graft vs Host Disease
Humans
Immunoglobulin Fab Fragments
Isoantigens
Lymphocyte Activation
Lymphocyte Count
Lymphocyte Depletion
Lymphopenia
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Transgenic
Receptors, Antigen, T-Cell
T-Lymphocyte Subsets
T-Lymphocytes, Cytotoxic
