HL-A 27 AND ARTHROPATHIES ASSOCIATED WITH ULCERATIVE COLITIS AND PSORIASIS
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Autoimmune alleles at the major histocompatibility locus modify melanoma susceptibility
2023, American Journal of Human GeneticsAxial psoriatic arthritis: An update for dermatologists
2021, Journal of the American Academy of DermatologyCitation Excerpt :Uveitis has been identified as a risk factor for PsA, but its role as a risk factor for axial involvement remains unclear.39 A notable risk factor for axial PsA is the presence of HLA-B27.36,40 HLA-B27 is a known key genetic marker of ankylosing spondylitis (AS), is present in more than 80% of patients with AS, and is the only known genetic marker common to AS and axial PsA.41
Implications of the diversity of class I HLA associations in psoriatic arthritis
2016, Clinical ImmunologyCitation Excerpt :The spondylitis group of diseases provides an intriguing counterpoise to the predominant class II MHC associated autoimmune disease that they do not reflect the biologic function of the CD4 T cell. The pioneering identification that certain HLA-B*27 alleles were strongly associated with ankylosing spondylitis susceptibility was the basis of this distinction, although how these alleles accomplish this is still not clearly understood [6,7]. The fact that psoriatic arthritis and reactive arthritis/Reiter's syndrome could appear in the setting of the severe immunodeficiency of AIDS with nearly complete depletion of CD4 T cells was a tragic experiment of nature that clearly etched the conclusion that the pathogenesis of the spondylitis group of diseases was completely different from autoimmune diseases such as RA or SLE, and presumably depended on the unregulated persisting CD8 T cell clones that were highly expanded in the ultimately unsuccessful effort HIV and other secondary pathogens [8,9]. This led to the paradigm that the genesis of the spondylitis group of diseases is the recognition by a CD8 T cell of a self-peptide presented by a class I MHC molecule, consistent with the lack of association of an autoantibody response with the diseases of this group [8,9]. This enkindled interest in the spondylitis group of diseases and, in turn, led to a collaboration of investigators at Columbia led by Robert Winchester with Oliver FitzGerald and his colleagues in the Dublin group to use sequence-based HLA typing to study the genotype of a meticulously phenotyped cohort of Irish psoriatic arthritis patients [10].
Arthritides
2013, Clinical Imaging: With Skeletal, Chest, & Abdominal Pattern Differentials: Third EditionSeronegative spondyloarthritis
2010, Best Practice and Research: Clinical RheumatologyCitation Excerpt :This pattern of increased mortality is similar to that seen with other inflammatory joint diseases [90–92], raising issues of the role of chronic inflammation in particular as regards cardiovascular mortality across the spectrum. PsA, like the other SpAs, is associated with HLA-B27 [93], predominantly in those individuals with axial symptoms of sacroiliitis or spondylitis (60–70% are HLA-B27 positive) [94–96]. The association is much weaker in predominantly peripheral PsA (24%) [94–96], and no increase in the frequency of HLA-B27 is seen in psoriasis alone (with the exception of pustular psoriasis) [97].
Human Leukocyte Antigen B27-Negative Axial Spondyloarthritis: What Do We Know?
2023, ACR Open Rheumatology