HLA Class I, II, and III Polymorphism in Italian Patients With Sarcoidosis: Conclusion

HLA Class I, II, and III Polymorphism in Italian Patients With Sarcoidosis: ConclusionWith regard to the association of HLA-radiologic stage of sarcoidosis, the most important deviations have been found in the group of patients in stage I (Table 3). HLA-B8,DR3 shows a higher frequency in stage I with respect to healthy control subjects and patients with stage III sarcoid. We are reminded that HLA-B8 seems to be associated with a good prognosis, and it could not be a simple coincidence if people possessing this allele belong to the radiologic stage I, in which a good outcome is more frequent with respect to other radiologic stages.
Concerning sex of patients and extent of the disease, we noticed several interesting associations, but none of these reached the significance when the p value was corrected for the number of antigens tested. cialis professional 20 mg

The second main purpose of our work was to investigate the possible association of sarcoidosis-MHC class III proteins, not yet studied in sarcoidosis. The HLA class III proteins (BF and C4 products) are fundamental components of the serum complement cascade acting on C3. It was suggested that the susceptibility or the resistance toward a disease with suspected immune component could be related to varying efficiency of immune aggregate dissolution. This fact, in turn, can depend on the strength of interaction of the polymorphic forms of C4 with other proteins in the complement activation. So we performed the study of these polymorphisms for at least two reasons: (1) to define particular HLA supratypes implicated in the disease, and (2) to investigate whether an immune deficiency can be due to the presence of silent allele as C4AQ0 or C4BQ0. But the latter is not the case in sarcoidosis, where we did not find increased frequencies of C4 null alleles, as in other diseases, such as systemic lupus erythematosus, where the fourth complement components deficiency seems to influence the dissolution and the removal of immune aggregates.
In conclusion, our report further supports the hypothesis of an involvement of immunogenetic factors in the pathogenesis and clinical presentation of sarcoidosis. That involvement would be of particular relevance if we consider that, as suggested by Israel and colleagues, factors other than initial intensity of lung inflammation, such as erythema nodosum, extra-thoracic spread, and race may be deeply involved in determining the ultimate outcome of sarcoidosis. Compared with other diseases, the association of HLA-sarcoidosis, however, seems to be rather weak. Molecular biology techniques in the near future will give a complete spectrum of H LA-linked genes associated with diseases, sarcoidosis included. However, preliminary results obtained by some of us failed to demonstrate that HLA DP 2.1 gene, an allele related to chronic beryllium disease, may be associated with sarcoidosis.

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