Difference in CD22 molecules in human B cells and basophils.

OBJECTIVE: CD22 is believed to be restricted to normal and neoplastic B cells. Human basophils were found to express CD22 molecules. Among the antibodies against CD22, Leu14, which recognized the ligand binding domain, reacted to basophils, and B3 and 4KB128, which recognized the amino terminus side and carboxy terminus side of the ligand binding epitope, respectively, did not. To clarify the difference of CD22 antigenicity in human B cells and basophils, we investigated RNA sequence and structures of CD22 molecules. MATERIALS AND METHODS: Purified B cells and basophils were obtained from normal human volunteers by using a MACS magnetic cell sorting system and anti-CD19 and anti-Fc epsilon R1 antibodies, respectively. RT-PCR and sequencing of CD22 mRNA were performed in the exons 3 to 8. Western blotting analysis of CD22 was also performed. RESULTS: The sequence of CD22 mRNA extracted from the basophils was the same as that of B cells in exons 3 to 8 (epitopes recognized by Leu14, B3, and 4KB128 were translated from exons 4 and 5). Reduced CD22 peptide extracted from the basophils reacted to Leu14 as well as B3 and 4KB128, and the molecular size of the reduced and nonreduced products was 130 kDa as expected. CONCLUSION: Disulfide bonds and the resulting 3D conformation of the CD22 molecules may have important roles in the difference of antigenicity of CD22 beta in B cells (CD22 beta 1) and basophils (CD22 beta 2). The difference in molecular structure surrounding the ligand-binding domain of CD22 may imply a specialization of the conformational forms of CD22 according to the ligand isoforms.

Cutaneous lymphoblastic lymphoma of putative plasmacytoid dendritic cell-precursor origin: two cases.

Although the neoplasm of relatively mature type plasmacytoid dendritic cells (pDC) was recently reported, that of pDC-precursor has not yet been defined. We experienced two elderly male Japanese patients with reddish skin tumors. The histology of the tumors in both patients showed terminal deoxinucleotidyl transferase (TdT)-positive lymphoblastic lymphoma (LBL). The pathological cells did not express T, B or NK markers, and no rearranged bands were shown for immunoglobulin (Ig)-JH, T cell receptor (TCR)-C beta, J gamma, J delta1, and c-myc. In addition, no Epstein-Barr virus (EBV)-derived DNA was detected in either case. The cells were (CD45, CD43, CD74, CD10, and HLA-DR)-positive in both cases, and one of the cases showed (CD4, CD36, CD54, CD58 and CD86)-positive plasmacytoid lymphoblasts, which appeared to be compatible with intermediate cells between human bone marrow lymphoid precursors and mature lymphoid DC. The cutaneous LBL in the two cases may, therefore, have been of pDC-precursor origin.

Long-term production of pre-existing alloantibodies to E and c after allogenic BMT in a patient with aplastic anemia resulting in delayed hemolytic anemia.

BACKGROUND: Delayed hemolysis mediated by long-term production of pre-existing recipient-derived antibodies directed against donor RBC antigens after allogenic BMT is an unusual complication of hematopoietic transplantation. CASE REPORT: A 26-year-old man with aplastic anemia had pre-existing alloantibodies to E and c. He received BMT from a donor, whose Rh phenotype was E+, c+. From about 1 month after the transplant, he showed mild hemolysis due to the antibodies. RESULTS: The patient was typed as group B, CCDee and had anti-E and c alloantibodies before BMT. The donor was typed as group O, ccDEE. Although MNCs from the donor marrow were infused into the patient, DAT became positive on Day 21, and the patient-origin antibodies remained detectable by both DAT and IAT even 20 months after BMT. However, immunomagnetically isolated peripheral circulating B cells were 100 percent donor origin. The patient received prednisolone from Day 221, and thereafter, the signs of hemolysis disappeared. CONCLUSION: It is likely that the long-term production of alloantibodies is due to the existence of long-lived recipient plasma cells, which survive the conditioning regimen. This case suggests that patients with pre- existing alloantibodies that do not belong to the ABO system should be carefully followed up after BMT.