scholarly journals T-cell receptor binding affinities and kinetics: impact on T-cell activity and specificity

Immunology ◽  
2009 ◽  
Vol 126 (2) ◽  
pp. 165-176 ◽  
Author(s):  
Jennifer D. Stone ◽  
Adam S. Chervin ◽  
David M. Kranz
Author(s):  
Kurt H. Piepenbrink ◽  
Brian E. Gloor ◽  
Kathryn M. Armstrong ◽  
Brian M. Baker

1991 ◽  
Vol 174 (4) ◽  
pp. 891-900 ◽  
Author(s):  
S M Friedman ◽  
M K Crow ◽  
J R Tumang ◽  
M Tumang ◽  
Y Q Xu ◽  
...  

While all known microbial superantigens are mitogenic for human peripheral blood lymphocytes (PBL), the functional response induced by Mycoplasma arthritidis-derived superantigen (MAM) is unique in that MAM stimulation of PBL consistently results in T cell-dependent B cell activation characterized by polyclonal IgM and IgG production. These immunostimulatory effects of MAM on the humoral arm of the human immune system warranted a more precise characterization of MAM-reactive human T cells. Using an uncloned MAM reactive human T cell line as immunogen, we have generated a monoclonal antibody (mAb) (termed C1) specific for the T cell receptor V beta gene expressed by the major fraction of MAM-reactive human T cells, V beta 17. In addition, a V beta 17- MAM-reactive T cell population exists, assessed by MAM, induced T cell proliferation and cytotoxic T cell activity. mAb C1 will be useful in characterizing the functional properties of V beta 17+ T cells and their potential role in autoimmune disease.


2007 ◽  
Vol 373 (2) ◽  
pp. 315-327 ◽  
Author(s):  
Peter J. Miller ◽  
Yael Pazy ◽  
Brian Conti ◽  
David Riddle ◽  
Ettore Appella ◽  
...  

2004 ◽  
Vol 279 (37) ◽  
pp. 38571-38576 ◽  
Author(s):  
Heather M. Baker ◽  
Thomas Proft ◽  
Phillip D. Webb ◽  
Vickery L. Arcus ◽  
John D. Fraser ◽  
...  

2000 ◽  
Vol 276 (8) ◽  
pp. 5659-5667 ◽  
Author(s):  
Yi Xiong ◽  
Petra Kern ◽  
Hsiu-Ching Chang ◽  
Ellis L. Reinherz

Immunity ◽  
1999 ◽  
Vol 10 (2) ◽  
pp. 227-237 ◽  
Author(s):  
S.Munir Alam ◽  
G.Mark Davies ◽  
Christina M. Lin ◽  
Tomasz Zal ◽  
Wade Nasholds ◽  
...  

2019 ◽  
Vol 88 (3) ◽  
pp. 503-513 ◽  
Author(s):  
Nishant K. Singh ◽  
Esam T. Abualrous ◽  
Cory M. Ayres ◽  
Frank Noé ◽  
Ragul Gowthaman ◽  
...  

2001 ◽  
Vol 194 (8) ◽  
pp. 1043-1052 ◽  
Author(s):  
Phillip D. Holler ◽  
Alice R. Lim ◽  
Bryan K. Cho ◽  
Laurie A. Rund ◽  
David M. Kranz

T cells are activated by binding of the T cell receptor (TCR) to a peptide-major histocompatibility complex (MHC) complex (pMHC) expressed on the surface of antigen presenting cells. Various models have predicted that activation is limited to a narrow window of affinities (or dissociation rates) for the TCR–pMHC interaction and that above or below this window, T cells will fail to undergo activation. However, to date there have not been TCRs with sufficiently high affinities in order to test this hypothesis. In this report we examined the activity of a CD8-negative T cell line transfected with a high affinity mutant TCR (KD = 10 nM) derived from cytotoxic T lymphocyte clone 2C by in vitro engineering. The results show that despite a 300-fold higher affinity and a 45-fold longer off-rate compared with the wild-type TCR, T cells that expressed the mutant TCRs were activated by peptide. In fact, activation could be detected at significantly lower peptide concentrations than with T cells that expressed the wild-type TCR. Furthermore, binding and functional analyses of a panel of peptide variants suggested that pMHC stability could account for apparent discrepancies between TCR affinity and T cell activity observed in several prior studies.


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