Molecular Basis for Recognition of an Arthritic Peptide and a Foreign Epitope on Distinct MHC Molecules by a Single TCR1
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D. Fremont | P. Allen | I. Matsumoto | D. Basu | S. Horvath
[1] A. Smolyar,et al. The crystal structure of a T cell receptor in complex with peptide and MHC class II. , 1999, Science.
[2] C. Benoist,et al. Arthritis provoked by linked T and B cell recognition of a glycolytic enzyme. , 1999, Science.
[3] E. Unanue,et al. The lack of consensus for I-A(g7)-peptide binding motifs: is there a requirement for anchor amino acid side chains? , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[4] K. Wucherpfennig,et al. pH-dependent Peptide Binding Properties of the Type I Diabetes–associated I-Ag7 Molecule: Rapid Release of CLIP at an Endosomal pH , 1999, The Journal of experimental medicine.
[5] P. Allen,et al. A Kinetic Threshold between Negative and Positive Selection Based on the Longevity of the T Cell Receptor–Ligand Complex , 1999, The Journal of experimental medicine.
[6] K. Rajewsky,et al. From systemic T cell self-reactivity to organ-specific autoimmune disease via immunoglobulins. , 1999, Immunity.
[7] E. Appella,et al. Structural Evidence of T Cell Xeno-reactivity in the Absence of Molecular Mimicry , 1999, The Journal of experimental medicine.
[8] R. Dwek,et al. Crystal structures of two H-2Db/glycopeptide complexes suggest a molecular basis for CTL cross-reactivity. , 1999, Immunity.
[9] Hiroaki Ito,et al. Analysis of the Role of Variation of Major Histocompatibility Complex Class II Expression on Nonobese Diabetic (NOD) Peripheral T Cell Response , 1998, The Journal of experimental medicine.
[10] P. Allen,et al. A basis for alloreactivity: MHC helical residues broaden peptide recognition by the TCR. , 1998, Immunity.
[11] P. A. Peterson,et al. Structural basis of 2C TCR allorecognition of H-2Ld peptide complexes. , 1998, Immunity.
[12] W A Hendrickson,et al. Crystal structure of I-Ak in complex with a dominant epitope of lysozyme. , 1998, Immunity.
[13] P. A. Peterson,et al. Crystal structures of two I-Ad-peptide complexes reveal that high affinity can be achieved without large anchor residues. , 1998, Immunity.
[14] L R Pease,et al. Structural basis of plasticity in T cell receptor recognition of a self peptide-MHC antigen. , 1998, Science.
[15] E. Unanue,et al. Autoreactivity of T cells from nonobese diabetic mice: an I-Ag7-dependent reaction. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[16] D. Covell,et al. Differential contact of disparate class I/peptide complexes as the basis for epitope cross-recognition by a single T cell receptor. , 1997, Journal of immunology.
[17] V. Kouskoff,et al. Organ-Specific Disease Provoked by Systemic Autoimmunity , 1996, Cell.
[18] K. Wiesmüller,et al. Molecular basis for the recognition of two structurally different major histocompatibility complex/peptide complexes by a single T-cell receptor. , 1996, Proceedings of the National Academy of Sciences of the United States of America.
[19] E. Unanue,et al. A negatively charged anchor residue promotes high affinity binding to the MHC class II molecule I-Ak. , 1996, Journal of immunology.
[20] E. Unanue,et al. Appreciating the Complexity of MHC Class II Peptide Binding: Lysozyme Peptide and I‐Ak , 1996, Immunological reviews.
[21] P. Allen,et al. Endogenous altered peptide ligands can affect peripheral T cell responses , 1996, The Journal of experimental medicine.
[22] E. Unanue,et al. The class II MHC I-Ag7 molecules from non-obese diabetic mice are poor peptide binders. , 1996, Journal of immunology.
[23] L. Pease,et al. Alloreactive 2C T cells recognize a self peptide in the context of the mutant Kbm3 molecule. , 1995, Journal of immunology.
[24] M. González-Gay,et al. Could HLA-DRB1 be the protective locus in rheumatoid arthritis? , 1995, Immunology today.
[25] J. Rothbard,et al. Specific T cell recognition of minimally homologous peptides: evidence for multiple endogenous ligands. , 1995, Immunity.
[26] J. Freed,et al. Comparison of peptides bound to spleen and thymus class II , 1993, The Journal of experimental medicine.
[27] C. Weyand,et al. The Influence of HLA-DRB1 Genes on Disease Severity in Rheumatoid Arthritis , 1992, Annals of Internal Medicine.
[28] R. Winchester. Genetic Determination of Susceptibility and Severity in Rheumatoid Arthritis , 1992, Annals of Internal Medicine.
[29] S. Hedrick,et al. Involvement of the same region of the T cell antigen receptor in thymic selection and foreign peptide recognition. , 1992, Journal of immunology.
[30] C. Benoist,et al. Delineation of antigen contact residues on an MHC class II molecule. , 1990, The EMBO journal.
[31] R. Holmdahl,et al. Structures on the I‐A molecule predisposing for susceptibility to type II collagen‐induced autoimmune arthritis , 1990, European journal of immunology.
[32] P. Allen,et al. Reconstruction of the immunogenic peptide RNase(43-56) by identification and transfer of the critical residues into an unrelated peptide backbone , 1989, The Journal of experimental medicine.
[33] D. Stage,et al. HLA genes associated with rheumatoid arthritis. Identification of susceptibility alleles using specific oligonucleotide probes. , 1989, Arthritis and rheumatism.
[34] David M. Kranz,et al. Positive and negative selection of an antigen receptor on T cells in transgenic mice , 1988, Nature.
[35] J. Todd,et al. A molecular basis for MHC class II--associated autoimmunity. , 1988, Science.
[36] M. A. Saper,et al. The foreign antigen binding site and T cell recognition regions of class I histocompatibility antigens , 1987, Nature.
[37] M. Gurney,et al. Molecular cloning and expression of neuroleukin, a neurotrophic factor for spinal and sensory neurons. , 1986, Science.
[38] H. Grey,et al. Antigen recognition by H-2-restricted T cells. I. Cell-free antigen processing , 1983, The Journal of experimental medicine.
[39] C. Werning. [Rheumatoid arthritis]. , 1983, Medizinische Monatsschrift fur Pharmazeuten.
[40] J. Dausset. GENETICS OF THE MAJOR HISTOCOMPATIBILITY COMPLEX , 1976 .
[41] S. Paget,et al. Predominantly T-cell infiltrate in rheumatoid synovial membranes. , 1975, The New England journal of medicine.