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B cells expressing CD5 antigen are markedly increased in peripheral blood and spleen lymphocytes from patients with immune thrombocytopenic purpura
Author(s) -
Mizutani Hajime,
Furubayashi Takayasu,
Kashiwagi Hirokazu,
Honda Shigenori,
Take Hironori,
Kurata Yoshiyuki,
Yonezawa Takeshi,
Tarui Seiichiro
Publication year - 1991
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1991.tb04475.x
Subject(s) - cd5 , thrombocytopenic purpura , spleen , autoantibody , medicine , immunology , antibody , immune system , platelet , antigen , b cell
Summary By two‐colour flow cytometric analysis, we examined the proportion of B lymphocytes bearing CD5 cell surface antigen (CD 5+ B cells), which are capable of producing autoantibodies, both in peripheral blood and spleen from patients with chronic immune thrombocytopenic purpura (ITP). The percentage of CD5+ B cells in peripheral blood lymphocytes (PBLs) was significantly increased ( P <0.005) in patients with ITP (3.7 ± 2.2%, n =30) as compared with normal controls (1.7 ± 0.7%, n =28). However, there was no correlation between the percentages of circulating CD5+ B cells and platelet counts: The percentage of splenic CD5+ B cells in ITP patients was much more increased (9.0 ± 4.5%, n =9), P <0.005) compared with that of other disorders (3.2 ± 0.5%, n =5). Furthermore, isolated splenic CD5+ B cells from two out of five ITP patients produced high levels of IgM‐type, platelet‐bindable antibodies (PBIgM) after stimulation with Staphylococcus aureus Cowan I (SAC), while CD5‐ B cells isolated from the same spleen or splenic CD5+ B cells from other non‐autoimmune disorders failed to produce significant amount of PBIgM. In three ITP patients, no increase in PBIgM was detected despite SAC stimulation. The increased proportion of CD5+ B cells in peripheral blood and spleen, and their ability to produce anti‐platelet antibodies indicate that they are directly involved in the autoimmune pathogenesis in ITP.