Infection and AutoimmunityYehuda Shoenfeld, Nancy Agmon-Levin, Noel R. Rose Infection and Autoimmunity encompasses the different mechanisms involved in the infection-autoimmunity association/induction. Special attention is given to heat shock proteins (HSPs) and to transgenic mouse models to better understand infection-induced autoimmunity. Organized into six parts, this book first discusses the mechanisms of autoimmune induction by infection. Some chapters follow discussing the vaccination and vaccines, including the controversial issue of vaccine-autoimmunity relationship. Other chapters elucidate the relationship of bacteria and parasites to autoimmunity. Lastly, the aspects of infections and diseases are described. This reference material will help readers gain a deeper insight into the important etiological aspects of autoimmunity.
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From inside the book
Results 1-5 of 76
Page 7
... binding by MHC class II molecules demonstrated that five peptide side chains contributed to binding [4]. However, each of these 'anchor residues' could typically be substituted by a number of other amino acids so that the resulting ...
... binding by MHC class II molecules demonstrated that five peptide side chains contributed to binding [4]. However, each of these 'anchor residues' could typically be substituted by a number of other amino acids so that the resulting ...
Page 8
... binding events: high affinity binding of peptide to an MHC molecule and the more shortlived association of TCR with this MHC/peptide surface. We decided to base our strategy on the minimal structural requirements for each of these two ...
... binding events: high affinity binding of peptide to an MHC molecule and the more shortlived association of TCR with this MHC/peptide surface. We decided to base our strategy on the minimal structural requirements for each of these two ...
Page 9
... binding as well as TCR recognition of the HLA-DR2/ MBP peptide complex. The MBP peptide is bound in an extended conformation as a type II polyproline helix and MBP peptide side chains occupy the P1, P4, P6 and P9 pockets of the binding ...
... binding as well as TCR recognition of the HLA-DR2/ MBP peptide complex. The MBP peptide is bound in an extended conformation as a type II polyproline helix and MBP peptide side chains occupy the P1, P4, P6 and P9 pockets of the binding ...
Page 10
... binding site. This large and hydrophobic pocket is occupied by P4 Phe of the MBP peptide. The necessary room for ... binding site (Table 1). This analysis shows that the HLA-DR2 contact surface of this set of peptides is highly diverse ...
... binding site. This large and hydrophobic pocket is occupied by P4 Phe of the MBP peptide. The necessary room for ... binding site (Table 1). This analysis shows that the HLA-DR2 contact surface of this set of peptides is highly diverse ...
Page 11
... binding studies, which indicated that only two positions of the peptide (P1 and P4) were critical for binding and that they could be substituted with other aliphatic residues or phenylalanine (P1 pocket) or other hydrophobic residues ...
... binding studies, which indicated that only two positions of the peptide (P1 and P4) were critical for binding and that they could be substituted with other aliphatic residues or phenylalanine (P1 pocket) or other hydrophobic residues ...
Contents
1 | |
5 | |
85 | |
121 | |
Bacteria and Autoimmunity | 319 |
Parasites and Autoimmunity | 437 |
Infection and Diseases | 471 |
Subject Index | 741 |
Other editions - View all
Infection and Autoimmunity Yehuda Shoenfeld,Nancy Agmon-Levin,Noel Richard Rose,Y. Shoenfeld Limited preview - 2004 |
Common terms and phrases
activation acute agents animals anti antibodies antigens arthritis Arthritis Rheum associated autoantibodies autoimmune disease bacterial binding blood cause cells chronic Clin clinical clones common complex controls cross-reactive cytokines damage demonstrated detected determined diabetes effects epitope et al evidence experimental expression factor frequency function gene genetic heart hepatitis host human immune response Immunol important increased individuals induced infection inflammatory initial involved lead levels liver lymphocytes major mechanisms mice molecular mimicry molecules multiple sclerosis myocarditis myosin Nature normal observed occur pathogenesis patients peptide peripheral persistent possible present production protein pylori reactive recent receptor recognized reported rheumatic fever risk role sequence serum severe showed shown similar specific spreading stimulation suggested syndrome synovial fluid T-cell therapy thyroid tion tissue treatment trigger type 1 diabetes vaccine vasculitis viral viral infection virus viruses
Popular passages
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