Analysis of T cell epitopes in the patients with the antiphospholipid syndrome.

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I) Efforts were made to establish monoclonal anti-βィイD22ィエD2-GPI and anti-prothrombin antibodies from peripheral blood lymphocytes of patients with antiphospholipid syndrome (APS).ii) A random peptide library was screened to identify the B cell epitope of anti-βィイD22ィエD2-GPI antibodies established from APS patients. Putative epitopes were identified on domain IV of the βィイD22ィエD2-GPI protein.iii) Among the known polymorphisms of βィイD22ィエD2-GPI, ィイD1247ィエD1Val/Leu polymorphism was associated with prevalence of anti-βィイD22ィエD2-GPI antibodies. A monoclonal anti-βィイD22ィエD2-GPI antibody was found to bind to ィイD1247ィエD1ValβィイD22ィエD2-GPI more strongly than to ィイD1247ィエD1LeuβィイD22ィエD2-GPI.iv) Peripheral blood T lymphocytes from APS were tested for their response against ィイD1247ィエD1ValβィイD22ィエD2-GPI and ィイD1247ィエD1LeuβィイD22ィエD2-GPI. A large heterogeneity was observed among individual patients, suggesting the importance of this polymorphism in βィイD22ィエD2-GPI induced T cell response.v) Two families with βィイD22ィエD2-GPI deficiency were identified. βィイD22ィエD2-GPI deficient individuals had a homozygous deletion in the 4ィイD1thィエD1 exon of βィイD22ィエD2-GPI. βィイD22ィエD2-GPI deficient individuals did not show significant abnormalities in hemostasis or lipid metabolism. Persons with hetorozygous deficiency were found in 6.3% of the studied population.