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A novel pathway of human B cell activation initiated by CK226 surface antigen
Author(s) -
Poggi Alessandro,
Maggi Enrico,
Biagiotti Roberta,
Giudizi Maria Grazia,
Almerigogna Fabio,
Pella Nicoletta,
Caligariscappio Federico,
Romagnani Sergio,
Moretta Lorenzo
Publication year - 1990
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830200532
Subject(s) - biology , microbiology and biotechnology , antigen , immunology
Abstract In this study we analyzed the effect of CK226 monoclonal antibody (mAb) on human B cell activation and proliferation. This mAb was shown to recognize a 75‐kDa surface molecule expressed on both T and B lymphocytes and to mediate T lymphocyte activation andproliferation. Flow cytometry analysis of B cell populations isolated from peripheral blood, tonsil and spleen showed that CK226 surface antigen is highly expressed on 40—80% of surface Ig + cells. When purified B cells were cultured in the presence of CK226 mAb, up‐regulation of major histocompatibility complex class II and CD23 surface structures and the de novo expression of CD25 antigen could be detected within 48 h. In addition, B cells underwent proliferation ([ 3 H] thymidine uptake) in the absence of either T cells or exogenous lymphokines. Proliferation was potentiated by the addition of suboptimal concentrations (0.5 ng/ml) of phorbol 12‐myristate 13‐acetate (PMA). Cells recovered at day 5 were surface Ig + and no CD3 + cells could be detected. CK226‐induced proliferation (either in the presence or in the absence of PMA) was not inhibited by anti‐CD25 mAb. Addition of exogenous interleukin 2 to CK226‐stimulated B cells resulted in further increase of B cell proliferation. On the other hand, CK226 mAb did not display a co‐stimulatory effect with submitogenic concentrations of either anti‐Ig antibody or Staphylococcus aureus Cowan strain I bacteria. In addition proliferation induced by mitogenic concentrations of the above stimuli was inhibited in a dose‐dependent fashion by CK226 mAb.