• During this time, the perception of CD has changed from a rather uncommon enteropathy to a common multi- organ disease with a strong genetic predisposition that is associated mainly with human leukocyte antigen (HLA)-DQ2 and HLA-DQ8. (vdocuments.net)
  • Methods Homocitrullinated peptides were identified and assessed in vitro for HLA-A2 binding and in vivo in human leukocyte antigen (HLA) transgenic mouse models for immunogenicity. (bmj.com)
  • Because the antigenic epitope is hidden within the triple helix of the collagen, an environmental factor (eg, smoking, hydrocarbon exposure) presumably is required to unmask the cryptic antigen to the immune system. (medscape.com)
  • Definitions CD is an immune-mediated systemic disorder elicited by gluten and related prolamines in genetically susceptible individuals and characterised by the presence of a variable combination of gluten-dependent clinical manifestations, CD-specific antibodies, Received and accepted September 1, 2011. (vdocuments.net)
  • Background Post-translational modification of proteins has the potential to alter the ability of T cells to recognize major histocompatibility complex (MHC) class -I and class-II restricted antigens, thereby resulting in altered immune responses. (bmj.com)
  • The HLA molecules and their counterparts in rodents were subsequently shown to be directly responsible for immune response differences between individuals and for determining the likelihood of graft rejection. (musculoskeletalkey.com)
  • The allelic variations among different HLA molecules are a major factor accounting for differences in the types of antigenic peptides to which an individual responds or in the types of T cells that are used in an immune response. (musculoskeletalkey.com)
  • Modified peptides showed enhanced binding to HLA-A2 compared with the native sequences and immunization of HLA-A2 transgenic mice generated high avidity modification specific CD8 responses that killed peptide expressing target cells. (bmj.com)
  • The syndrome was subsequently shown to be caused by an antibody response against antigens present in the alveolar and glomerular basement membranes. (medscape.com)
  • IgA and IgG responses, meanwhile, like those seen to anti-gliadin antibodies in celiac disease or dermatitis herpetiformis, are not seen in response to avenins in atopic dermatitis patients. (wikipedia.org)
  • All three patients were the DQ2.5/DQ2 (HLA DR3-DQ2/DR7-DQ2) phenotype. (wikipedia.org)
  • In 1967, in a classic experiment, Lerner and colleagues transferred anti-GBM disease to monkeys by injecting them with kidney-bound antibodies from patients with anti-GBM nephritis. (medscape.com)
  • Antibodies reacting with the alpha-3 chain of type IV collagen can be detected in the serum and can be eluted from kidneys of patients with anti-GBM nephritis. (medscape.com)
  • Approximately 20-40% of patients positive for anti-GBM antibodies also have antineutrophilic cytoplasmic antibodies (ANCAs). (medscape.com)
  • The 2004 National Institutes of Health/ Agency for Healthcare Research and Quality report and a systematic literature search on antibody tests for CD in paediatric patients covering the years 2004 to 2009 was the basis for the evidence-based recommendations on CD-specific antibody testing. (vdocuments.net)
  • When bound to the specific antigens in the kidneys and lungs, the antibodies initiate an inflammatory destruction of tissues by complement activation and recruitment of proinflammatory cells, leading to rapidly proliferative glomerulonephritis, often accompanied by pulmonary hemorrhage. (medscape.com)
  • The polymorphisms associated with the "shared epitope" are located on the α-helical rim (DRB1 chain) of the peptide-binding cleft, where they may interact with either the bound peptide antigen or the T cell receptor. (musculoskeletalkey.com)
  • Interestingly, the recent data in RA indicate that the major HLA-DR associations are with anti-CCP antibody positive disease, suggesting that control of autoantibody responses may be a primary mechanism underlying these associations in RA as well. (musculoskeletalkey.com)
  • citation needed] In gluten-sensitive enteropathy, prolamins mediate between T-cells and antigen-presenting cells, whereas anti-transglutaminase antibodies confer autoimmunity via covalent attachment to gliadin. (wikipedia.org)
  • In each individual, T cells are generally restricted to recognize antigens presented by the person's own HLA molecules. (musculoskeletalkey.com)
  • An early and precise diagnosis of anti-GBM disease is extremely important for preventing death and preserving renal function. (medscape.com)
  • The diagnosis of CD also has changed as a result of the availability of CD-specific antibody tests, based mainly on tissue transgluta- minase type 2 (TG2) antibodies. (vdocuments.net)
  • Anti-avenin antibodies declined in treated celiacs on an oat diet in 136 individuals, suggesting oats can be involved in celiac disease when wheat is present, but are not involved when wheat is removed from the diet. (wikipedia.org)
  • Anti-glomerular basement membrane (anti-GBM) disease is a classic autoimmune disorder characterized by the presence of circulating pathogenic autoantibodies directed against proteins in the glomerular and alveolar basement membranes. (medscape.com)
  • Go to Pediatric Anti-GBM Disease (Goodpasture Syndrome) for complete information on this topic. (medscape.com)
  • This distribution helps explains the specific organ involvement (ie, glomerulonephritis and pulmonary hemorrhage) in persons with anti-GBM nephritis. (medscape.com)
  • Once the anti-GBM antibodies bind to the specific GBM antigen, complement is activated. (medscape.com)
  • In the case of systemic lupus erythematosus (SLE) and related illnesses, many of the HLA class II alleles are associated with the presence of specific autoantibodies or clinical phenotypes. (musculoskeletalkey.com)
  • A follow-up study showed that most celiacs have anti-avenin antibodies (AVAs), with a specificity and sensitivity comparable to anti-gliadin antibodies. (wikipedia.org)
  • HLA class I molecules consist of a 45-kD α chain encoded within the MHC that is noncovalently associated with the 12-kD β 2 -microglobulin chain (encoded on chromosome 15). (musculoskeletalkey.com)
  • HLA class II molecules consist of noncovalently associated α (32 kD) and β (28 kD) chains, both of which are encoded within the MHC. (musculoskeletalkey.com)
  • HLA class I and class II molecules are cell surface glycoproteins, anchored to the membrane by hydrophobic transmembrane segments. (musculoskeletalkey.com)
  • Over the years, tremendous gains have been made in knowledge of the pathogenic mechanisms underlying anti-GBM nephritis. (medscape.com)
  • IgA and IgG responses, meanwhile, like those seen to anti-gliadin antibodies in celiac disease or dermatitis herpetiformis, are not seen in response to avenins in atopic dermatitis patients. (wikipedia.org)
  • Anti-avenin antibodies declined in treated celiacs on an oat diet in 136 individuals, suggesting oats can be involved in celiac disease when wheat is present, but are not involved when wheat is removed from the diet. (wikipedia.org)
  • Celiac disease is a multifactorial disorder resulting from the interaction of HLA-DQA1 and HLA-DQB1 allelic variants known to be associated with celiac disease susceptibility, less well-recognized variants in non-HLA genes, gliadin (a subcomponent of gluten), and other environmental factors. (nih.gov)
  • A follow-up study showed that most celiacs have anti-avenin antibodies (AVAs), with a specificity and sensitivity comparable to anti-gliadin antibodies. (wikipedia.org)
  • citation needed] In gluten-sensitive enteropathy, prolamins mediate between T-cells and antigen-presenting cells, whereas anti-transglutaminase antibodies confer autoimmunity via covalent attachment to gliadin. (wikipedia.org)
  • The disease is featured by a variable combination of clinical signs, specific antibodies, HLA-DQ2 and HLA-DQ8 haplotypes, and enteropathy. (wjgnet.com)
  • Several factors including age, gender, ethnicity, quality and quantity of vaccine antigen, doses, and route of administration can influence immune response to vaccination, although the main cause of variation in the responsiveness among vaccine recipients is host genetic variability. (wjgnet.com)
  • Human leukocyte antigen (HLA) haplotype DQ2 or DQ8 identified by molecular genetic testing of HLA-DQA1 and HLA-DQB1 . (nih.gov)
  • Further molecular genetics studies of HLA-DR2 reveal that the association of anti-GBM nephritis is with HLA-DRB1 alleles (HLA-DRB1 1501 and 1502 alleles), HLA-DQA1 01 alleles, and HLA-DQB1 06 alleles. (medscape.com)
  • Anti-GBM disease shows a strong association with HLA-DR2. (medscape.com)