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Table 19 3 Association between the presence of various HLA markers and selected autoimmune diseases
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Disease Ankylosing spondylitis Reactive arthropathy, including Reiter s syndrome Rheumatoid arthritis Beh et s syndrome Systemic lupus erythematosus Insulin-dependent (type 1) diabetes mellitus B27 B27 DR4 B51 DR3 DR3 DQB1*0201 DR4 DQB1*0302 DR2 DRB*15013 DRB*01013 DQB1*06023 Idiopathic Addison s disease Graves disease Hashimoto s disease Postpartum thyroiditis Celiac disease DR3 DR3 DR11 DR4 DR3 DQB1*02013 DQA1*05013 DR7,11 DR7, DQB1*02013 DR11, DQA1*05013 Dermatitis herpetiformis Sicca syndrome Myasthenia gravis Idiopathic membranous glomerulonephritis Goodpasture s syndrome Multiple sclerosis DR3 DR3 DR3 B8 DR3 DR2 DR2 DRB1*15013 DRB5*01013 DQB1*06023 Pemphigus vulgaris (among Ashkenazi Jews) Psoriasis vulgaris Birdshot retinochoroidopathy
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Associated HLA Marker1
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Relative Risk of Disease2 874 370 42 38 58 33 24 64 95 019
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Symbols with asterisks indicate alleles, and symbols without asterisks indicate serologically defined antigens For each disease, the marker or markers with the strongest associations are given In many cases in which it is difficult to decide whether HLA-DR or -DQ markers are responsible for association, both markers are given 2 The relative risk indicates the frequency of a disease in persons with the HLA marker as compared with persons without the marker A positive association (ie, when the HLA marker is more frequent in persons with the disease than in those without it) is indicated by a relative risk of more than 10, a negative association by a relative risk of less than 10, and no association by a relative risk of 10 3 The risk has not been assessed separately for this allele Reproduced, with permission, from Svejgaard A MHC and disease associations In: Herzenberg LA et al (editors) Weir s Handbook of Experimental Immunology, 5th ed Blackwell Science, 1996
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tant for long-term graft survival Grafts from cadaver donors with zero HLA mismatches have a half-life of 113 years Those with six mismatches have a half-life of 68 years, compared with those from HLA-identical siblings, which have a half-life of 236 years Some donors are highly sensitized to HLA antigens from previous transfusions, ie, possess high panel reactive antibody levels It may be difficult to find a suitable donor, since a positive cross-match by cytotoxicity testing is likely and would be a contraindication to transplant Donor screening is performed in all cases to assess suitability, rule out hypertension or anatomic anomalies, and avoid transmission of hepatitis viruses, HIV, and other infectious agents Owing to the scarcity of related donors, living unrelated donors may be used in certain circumstances Pretreatment of recipients with blood transfusions from the donor appears to extend graft survival even longer Delayed allograft function can be due to hyperacute graft rejection, postischemic acute tubular necrosis, cyclosporine toxicity, or obstructive nephropathy If conservative measures do not improve function or patients are at high risk for allograft rejection, renal biopsy should be performed for definitive diagnostic purposes Renal allograft rejection may be due to hyperacute rejection from binding of cytotoxic antibodies and complement activation, acute rejection from cellular immune responses, or chronic rejection A form of interstitial nephritis secondary to polyomavirus infection is associated with aggressive immunosuppression Noninvasive methods to diagnose rejection are being developed To replace the need for renal biopsy, studies of mRNA reveal that the levels of FOXP3 in urinary cells may serve as a mechanistically informative biomarker of acute rejection Chronic allograft nephropathy is characterized by vasculopathy and immune-mediated graft obliteration Previous acute rejection is strongly linked with later chronic rejection, and severity of those episodes has prognostic implications Cyclosporine-induced nephrotoxicity and recurrent or de novo renal disease are also significant factors affecting longterm survival Induction immunosuppressive regimens have been used to suppress acute rejection during the high-risk period, immediately following transplantation High doses of combined corticosteroids, calcineurins and antiproliferative agents or sirolimus may be used during the induction phase, or alternatively, T cell-depleting polyclonal or monoclonal antibodies may be used Maintenance immunosuppressive regimens are characterized by lower doses of immunosuppressive agents with the aim of preventing recurrent rejection and chronic nephropathy, prolonging graft survival, and minimizing potentially serious medication side effects
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