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Deciduous teeth affected by dentinogenesis imperfecta were obtained from two patients with osteogenesis imperfecta. Electron microscopy of the dentin revealed some structural alterations. The striation of the collagen fibrils was not clear, and the crystals were less dense than in normal detain. The amino acid analysis of dentin collagen was slightly different from normal dentin. There were slight increases in the amounts of hydroxylysine, serine and acidic acids. On the other hand, lysine and arginine were reduced. The elevation of hexosyllysine content and an increase of carbohydrate were also observed. These results indicate that either dentin collagen is altered, or noncollagenous matrices associated with collagen arc increased in dentinogenesis imperfecta dentin. [ABSTRACT FROM AUTHOR]

Problem: Tumor necrosis factor (TNF)-alpha is a major cytokine involved in inflammatory and immune function. The aim of this study was to investigate whether polymorphisms at positions -1031, -863 and -857 in the TNF gene promoter region (TNFA) and TNF receptor type 2 gene (TNFR2) are responsible in part for genetic susceptibility to endometriosis., Methods of Study: TNFA and TNFR2 polymorphisms were determined in 123 patients with endometriosis and 165 fertile healthy women by the polymerase chain reaction (PCR) - preferential homoduplex formation assay and PCR-restriction fragment length polymorphism, respectively., Results: The frequency of the TNFA-U01 haplotype was increased significantly in patients with endometriosis compared with controls (P = 0.045, OR = 1.45). The TNFA-U01 haplotype was strongly associated with HLA-B*0702. No difference was found in TNFR2 polymorphism between patients and controls., Conclusion: Our results indicated that TNFA promoter polymorphism was associated with susceptibility to endometriosis. However, this association was not independent of HLA-class I polymorphisms.

Problem: Interleukin-10 (IL-10) is an important immunomodulatory cytokine. The aim of this study was to investigate whether polymorphisms of the IL-10 gene promoter polymorphisms may be responsible in part for genetic susceptibility to endometriosis., Methods of Study: Polymorphisms at position -1082 and -592 in the IL-10 promoter region were determined in 196 patients with endometriosis and 160 fertile healthy women by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP)., Results: There were no statistically significant differences in the genotype and allele frequencies of IL-10 promoter polymorphism between the endometriosis and control groups. However, when subgrouped according to clinical features, the frequencies of the -592*CC genotype and -592*C allele were significantly increased in patients with autoantibodies to carbonic anhydrase II (anti-CA II ab) compared with controls., Conclusion: IL-10 promoter polymorphisms were associated with the production of anti-CA II ab in patients with endometriosis, suggesting a role in the genetic susceptibility for endometriosis.

Specific anti-human thymus xenoantiserum (ATS) was utilized for characterizing a human thymus antigen (HTA) preferentially expressed on human thymocytes. Binding of ATS with different cell types was studied by immunofluorescence and immunoperoxidase techniques, as well as by radioimmunoprecipitation (RIP) followed by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). ATS reacted selectively with the majority (87%) of human thymocytes among normal lymphoid cell populations tested. In the thymus, HTA was expressed largely on cortical thymocytes but not on those cells located in the thymic medulla. When 20 cases of different types of lymphatic leukemias were studied with ATS, HTA was found on acute lymphoblastic leukemia cells rosetting with sheep erythrocytes (T-ALL) but not on other lymphatic leukemia cases, including chronic lymphocytic leukemia cells rosetting with sheep red blood cells (T-CLL). SDS-PAGE analysis of immunoprecipitates formed between ATS and radiolabeled cell-surface components of human thymocytes demonstrated that ATS bound a 48,000-molecular-weight component that could be adsorbed to Sepharose 4B coupled with Les culinaris hemagglutinin and could be labeled by periodate-tritiated borohydride, indicating that HTA is a sialoglycoprotein. Similar antigen molecules were also precipitated by ATS from T-ALL cells but not from other lymphatic leukemia cells. Five T-ALL-derived cell lines were tested with ATS by immunofluorescence and by RIP and SDS-PAGE, but only two cell lines (MOLT-3 and P12/Ich) possessed HTA molecules on their cell membrane.

Leukemic cells from eight adult patients with various types of T-cell leukemias, including one patient with lymphosarcoma cell leukemia (T-LSL), two patients with chronic lymphocytic leukemia (T-CLL), and five patients with adult T-cell leukemia (ATL), were analyzed for their surface antigenic phenotypes with a series of monoclonal antibodies directing to human T-cell differentiation antigens. All of the leukemic T cells studied were regarded as being of post-thymic T-cell origin because of their ability to form rosettes with sheep red cells under the condition at 4 degrees C but not 37 degrees C as well as the expression of human Ly-1-like but not TL-like antigen on their cell surfaces. By using monoclonal antibodies to a variety of human of three distinct categories. Thus, one patient with T-LSL had cells with Leu-1+2a+3a+ phenotype, which might reflect possible post-thymic precursor T cells, whereas one patient with T-CLL had cells with the same phenotype (Leu-1+2a+3a-) as normal cytotoxic/suppressor T cells. The latter cells also expressed Ia antigens as defined by monoclonal antihuman Ia antibody. The remaining six cases, including one T-CLL and five ATL patients had leukemic cells with the same phenotype (Leu-1+2a-3a+) as normally found on helper/inducer T cells, despite distinct clinical and immunological features between T-CLL and ATL. Some clinical findings observed in those patients may reflect functional activities retained by their leukemic T cells.

A new monoclonal antibody specific for human B cell differentiation antigen (HLB-1) is produced by a hybridoma established by fusion of splenocytes of mice immunized with the Epstein-Barr virus (EBV)-transformed peripheral B cell line, RPMI-8057. This monoclonal, antibody designated anti-HLB-1 monoclonal antibody (anti-HLB-1), reacted with surface immunoglobulin (sIg)-positive B cells of normal peripheral blood and lymphoid tissues and sIg-positive leukemic cells. The cells of T cell leukemia, non-T non-B acute lymphoblastic leukemia (ALL) and nonlymphoid leukemia were HLB-1 negative. These data were further confirmed by studying a panel of cultured human hematopoietic cell lines. Anti-HLB-1 reacted with B cell lines derived from pre-B, Burkitt's lymphoma, B cell type ALL and EBV-transformed peripheral B cells. Anti-HLB-1 was reactive with only one of three human myeloma cell lines, and with none of the T cell, myeloid and non-T non-B ALL cell lines. This newly defined HLB-1 antigen is different from other conventional human B cell markers such as sIg, Ia antigens, and receptors for the Fc portion of Ig and complement C3.