Biased T-cell receptor usage is associated with allelic variation in the MHC class II peptide binding groove

1999 ◽  
Vol 49 (6) ◽  
pp. 532-540 ◽  
Author(s):  
B. Yassine-Diab ◽  
P. Carmichael ◽  
Fatima-Ezzahra L'Faqihi ◽  
Giovanna Lombardi ◽  
Sarah Deacock ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Allelic Variation ◽  
Peptide Binding ◽  
Cell Receptor ◽  
Class Ii ◽  
Receptor Usage ◽  
Peptide Binding Groove ◽  
Binding Groove

scholarly journals Structure of a Complex of the Human α/β T Cell Receptor (TCR) HA1.7, Influenza Hemagglutinin Peptide, and Major Histocompatibility Complex Class II Molecule, HLA-DR4 (DRA*0101 and DRB1*0401)

2002 ◽  
Vol 195 (5) ◽  
pp. 571-581 ◽  
Author(s):  
Jens Hennecke ◽  
Don C. Wiley
Keyword(s):  
Major Histocompatibility Complex ◽  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Peptide Binding ◽  
Cell Receptor ◽  
Class Ii ◽  
Histocompatibility Complex ◽  
Peptide Binding Groove ◽  
Binding Groove

The α/β T cell receptor (TCR) HA1.7 specific for the hemagglutinin (HA) antigen peptide from influenza A virus is HLA-DR1 restricted but cross-reactive for the HA peptide presented by the allo-major histocompatibility complex (MHC) class II molecule HLA-DR4. We report here the structure of the HA1.7/DR4/HA complex, determined by X-ray crystallography at a resolution of 2.4 Å. The overall structure of this complex is very similar to the previously reported structure of the HA1.7/DR1/HA complex. Amino acid sequence differences between DR1 and DR4, which are located deep in the peptide binding groove and out of reach for direct contact by the TCR, are able to indirectly influence the antigenicity of the pMHC surface by changing the conformation of HA peptide residues at position P5 and P6. Although TCR HA1.7 is cross-reactive for HA presented by DR1 and DR4 and tolerates these conformational differences, other HA-specific TCRs are sensitive to these changes. We also find a dependence of the width of the MHC class II peptide-binding groove on the sequence of the bound peptide by comparing the HA1.7/DR4/HA complex with the structure of DR4 presenting a collagen peptide. This structural study of TCR cross-reactivity emphasizes how MHC sequence differences can affect TCR binding indirectly by moving peptide atoms.

Vulnerability of allografts to rejection by MHC class II-restricted T-cell receptor transgenic mice1

2003 ◽  
Vol 75 (8) ◽  
pp. 1415-1422 ◽  
Author(s):  
Major K. Lee ◽  
Xiaolun Huang ◽  
Beth P. Jarrett ◽  
Daniel J. Moore ◽  
Niraj M. Desai ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii

scholarly journals MHC class II engagement inhibits CD99-induced apoptosis and up-regulation of T cell receptor and MHC molecules in human thymocytes and T cell line

FEBS Letters ◽  
2003 ◽  
Vol 546 (2-3) ◽  
pp. 379-384 ◽  
Author(s):  
Min Kyung Kim ◽  
Yoon-La Choi ◽  
Min Kyung Kim ◽  
Seok-Hyung Kim ◽  
Eun Young Choi ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Line ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii ◽  
Mhc Molecules ◽  
Induced Apoptosis

Structural basis for the recognition of mutant self by a tumor-specific, MHC class II–restricted T cell receptor

2007 ◽  
Vol 8 (4) ◽  
pp. 398-408 ◽  
Author(s):  
Lu Deng ◽  
Ries J Langley ◽  
Patrick H Brown ◽  
Gang Xu ◽  
Leslie Teng ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii ◽  
Structural Basis

T cell receptor recognition of MHC class II-bound peptide flanking residues results in altered Vβ usage and profound functional dependency

1997 ◽  
Vol 56 ◽  
pp. 6-7
Author(s):  
Richard T. Carson ◽  
Kate M. Vignali ◽  
David L. Woodland ◽  
Dario A.A. Vignali
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii ◽  
Functional Dependency ◽  
Receptor Recognition

scholarly journals Determination of Interaction Kinetics between the T Cell Receptor and Peptide-Loaded MHC Class II via Single-Molecule Diffusion Measurements

2012 ◽  
Vol 103 (2) ◽  
pp. L17-L19 ◽  
Author(s):  
Markus Axmann ◽  
Johannes B. Huppa ◽  
Mark M. Davis ◽  
Gerhard J. Schütz
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Single Molecule ◽  
Cell Receptor ◽  
Class Ii ◽  
Interaction Kinetics

T cell receptor usage in brains of multiple sclerosis patients. Correlation with HLA class II molecular phenotype

1991 ◽  
Vol 35 ◽  
pp. 31 ◽  
Author(s):  
J.R. Oksenberg ◽  
M.A. Panzara ◽  
M. Sherrit ◽  
A. Begovich ◽  
H. Erlich ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Class Ii ◽  
Hla Class Ii ◽  
Molecular Phenotype ◽  
Receptor Usage ◽  
Multiple Sclerosis Patients

scholarly journals Pathogenesis of an Infectious Mononucleosis-like Disease Induced by a Murine γ-Herpesvirus: Role for a Viral Superantigen?

1997 ◽  
Vol 185 (9) ◽  
pp. 1641-1650 ◽  
Author(s):  
Ralph A. Tripp ◽  
Ann Marie Hamilton-Easton ◽  
Rhonda D. Cardin ◽  
Phuong Nguyen ◽  
Frederick G. Behm ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Infectious Mononucleosis ◽  
Cd8 T Cells ◽  
Peripheral Blood ◽  
Cell Receptor ◽  
Class Ii ◽  
Congenic Mice

The murine γ-herpesvirus 68 has many similarities to EBV, and induces a syndrome comparable to infectious mononucleosis (IM). The frequency of activated CD8+ T cells (CD62Llo) in the peripheral blood increased greater than fourfold by 21 d after infection of C57BL/6J (H-2b) mice, and remained high for at least a further month. The spectrum of T cell receptor usage was greatly skewed, with as many as 75% of the CD8+ T cells in the blood expressing a Vβ4+ phenotype. Interestingly, the Vβ4 dominance was also seen, to varying extents, in H-2k, H-2d, H-2u, and H-2q strains of mice. In addition, although CD4 depletion from day 11 had no effect on the Vβ4 bias of the T cells, the Vβ4+CD8+ expansion was absent in H-2IAb–deficient congenic mice. However, the numbers of cycling cells in the CD4 antibody–depleted mice and mice that are CD4 deficient as a consequence of the deletion of MHC class II, were generally lower. The findings suggest that the IM-like disease is driven both by cytokines provided by CD4+ T cells and by a viral superantigen presented by MHC class II glycoproteins to Vβ4+CD8+ T cells.

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