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Collectively, our data suggest that the measurement of soluble HLA in body fluids can be of both diagnostic and prognostic value in the assessment of patients with autoimmune rheumatic disorders. The mechanism by which sHLA enters saliva is unclear, but they probably are not acquired from serum.

We correlated serum concentrations of soluble class I HLA antigens (S-HLA-I) with HLA allotypes in 82 unrelated Caucasian and 58 unrelated African-American putatively normal subjects, as well as in 31 individuals with stable, normally functioning liver transplants. Caucasian and African-American subjects with HLA-A23 or HLA-A24 were high secretors of S-HLA-I. We also observed that some HLA-A allotypes associated with high serum concentrations of S-HLA-I were ethnicity specific. HLA-A33 was associated with high S-HLA-I secretion in African-Americans but not in Caucasians. HLA-A29 was associated with high S-HLA-I secretion in Caucasians but not in African-Americans. All liver transplant recipients studied who were high secretors of S-HLA-I postoperatively carried HLA-A24 or HLA-A29. (There were no HLA-A33 or HLA-A23 allotypes in this group.) The "secretor genes," however, may be autogenous or allogenic (i.e., either donor or recipient HLA-A24 or HLA-A29 resulted in the observed high secretor status in liver transplant recipients after transplantation). It is noteworthy that serum S-HLA-I concentrations were low in all subjects with HLA-A2 regardless of whether the HLA-A2 was of recipient or donor origin. This finding suggests that HLA-A2 could have a suppressive effect on S-HLA-I secretion.

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Our objective was to study a possible contribution of major histocompatibility complex (MHC) genes to soluble HLA-I synthesis in patients with systemic lupus erythematosus (SLE). Solid-phase enzyme-linked immunoassay (ELISA) was used to measure sHLA-I in the sera of 20 patients with SLE and 76 normal controls with known HLA phenotypes. Serial serum samples ( n=108) from the above group of patients ( n=19) were further investigated by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting. Soluble HLA-I levels were abnormally higher in patients with SLE than normal controls ( P<0.0002). No complete HLA haplotype has been identified to be correlated with high or low sHLA-I secretion. Only the sera of HLA-A23- or -A24- (splits of HLA-A9) positive individuals were found to contain high sHLA-I concentrations in both populations studied. The difference between sHLA-I of HLA-A24 patients ( n=7) and HLA-A24 normal controls ( n=19) was statistically highly significant ( P<0.0079). The results suggest that HLA-A24 may confer additional risk of more severe disease expression in female patients with SLE. The data imply that SLE patients carrying 39-kDa sHLA-I have increased risk of developing renal disease. A higher prevalence of 35-37 kDa was observed in patients with mild disease. Interestingly, 44-46 kDa was the predominant molecular form of sHLA-I in SLE patients with lymphocytosis with no evidence of organ involvement. Notably, all these variations were not reflected by differences in HLA phenotypes, with the exception of HLA-A24-positive patients, in whom the 44-46-kDa form occurs consistently but not exclusively. In summary, the results show a genetic heterogeneity of SLE with MHC control of the expression of sHLA-I concentrations and possible involvement of disease-associated factors that might potentiate a specific sHLA-I molecule synthesis.

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