Adhesion molecule CD11a/CD18-deficient Burkitt's lymphoma cells lack the transcript for the beta, but not the alpha, integrin subunit.

Adhesion to cells and matrices participates in the regulation of lymphocyte proliferation, maturation and tissue localization. Consequently, abnormal patterns of adhesion molecule expression may contribute to the pathophysiology of lymphoproliferative disorders. Integrins are major cell-surface adhesive proteins composed by alpha and beta subunits. In contrast to normal lymphocytes, Burkitt's lymphoma (BL) cells lack the beta2 integrin CD11a/CD18. To study the molecular mechanism underlying this deficiency, presence of the transcript for each subunit was analysed by Northern blotting in group I BL lines (BL biopsy-like) and, for comparison, Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs). While transcripts for both CD11a (alpha subunit) and CD18 (beta subunit) were readily detected in LCLs, BL lines contained the transcript for the alpha subunit only. Treatment of BL cells with phorbol ester for 72 h induced expression of the beta subunit mRNA and the CD11a and CD18 antigens on the cell surface. The results indicate that the CD11a/CD18 deficiency of BL is due to absence of the beta subunit transcript and that this defect is restored by stimulation of the cells.