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A Role for L‐Selectin in Monocyte Activation by Jurkat Tumour Cells
Author(s) -
Putz E. F.,
MÄnnel D. N.
Publication year - 1996
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1996.d01-346.x
Subject(s) - jurkat cells , monoclonal antibody , monocyte , tumor necrosis factor alpha , microbiology and biotechnology , cell culture , sialic acid , selectin , biology , cytokine , t cell , chemistry , biochemistry , antibody , immunology , cell adhesion molecule , immune system , genetics
Monocytes and macrophages can distinguish between tumour cells and non‐malignant cells of the same cell type. The surface structures mediating tumour cell recognition and tumour cell‐induced cytokine production by monocytes or macrophages are still poorly characterized. The authors previously described N‐linked sialic acid‐containing carbohydrates associated with CD2 of the CD4 + tumour cell line Jurkat which induced tumour necrosis factor (TNF) secretion by human monocytes. In this report the authors demonstrate a role for monocytic L‐selectin in this process. Mannose‐6‐phosphate, an inhibitor of L‐selectin binding, blocked CD2‐induced TNF production whereas other ligands for L‐selectin (the monomeric monoclonal antibody to L‐selectin, DREG‐200; inositol hexaphosphoric acid; heparin) amplified CD2‐induced secretion of TNF. Polyvalent L‐selectin ligands as soluble monoclonal antibody (MoAb) DREG‐56, the cross‐linked MoAb DREG‐200, and the marine algal polysaccharide fucoidin induced TNF production without addition of CD2. Jurkat‐CD2 is associated with sialyl Lewis X‐related carbohydrates which differ in their expression or composition from that of the non‐stimulatory CD2 from non‐malignant T cells. Taken together the data presented in this report suggest that — at least in the case of Jurkat‐CD2 — L‐selectin is involved in monocyte activation by tumour typical carbohydrate structures.