TNF-alpha induces spreading of B-CLL via the CD11c/CD18 molecule

Am J Hematol. 1993 Dec;44(4):221-8. doi: 10.1002/ajh.2830440402.

Abstract

Activation of malignant B cells can lead to extensive morphological changes of these cells. A combination of PMA and TNF-alpha can induce adherence of purified B-CLL cells, which acquire a dendritic cell-like appearance. This phenomenon that we have termed spreading, is accompanied by upregulation of expression of both beta 1 and beta 2 integrin molecules. Spreading was inhibited by the addition of antibodies against CD18 or CD11c. In other B cell malignancies (HCL and NHL), morphological changes could be induced by PMA in the absence of TNF-alpha. Culturing in the presence of prednisolone resulted in an inhibition of spreading, most likely mediated via a down regulation of CD18 and CD11c expression. These data indicate that the CD11c/CD18 complex might be important for the adhesive properties of B cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, CD / drug effects
  • Antigens, CD / physiology*
  • B-Lymphocytes / drug effects
  • B-Lymphocytes / pathology*
  • CD11 Antigens
  • CD18 Antigens
  • Cell Adhesion / drug effects
  • Cell Division / drug effects
  • Culture Techniques / methods
  • Fluorescent Antibody Technique
  • Humans
  • Leukemia, Lymphocytic, Chronic, B-Cell / blood
  • Leukemia, Lymphocytic, Chronic, B-Cell / pathology*
  • Prednisone / pharmacology
  • Recombinant Proteins / pharmacology
  • Tetradecanoylphorbol Acetate / pharmacology
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Antigens, CD
  • CD11 Antigens
  • CD18 Antigens
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Tetradecanoylphorbol Acetate
  • Prednisone