Triggering of cytotoxic T lymphocytes and NK cells via the Tp103 pathway is dependent on the expression of the T cell receptor/CD3 complex.
The expression and function of the T cell activation molecule Tp103 on human cloned cytotoxic CD3+ and CD3- cells were studied. All in vitro growing CD3+ and CD3- clones expressed Tp103 regardless of their phenotype and the expression of a CD3-associated TCR complex. Whereas the CD2 pathway was functional in all these clones, only CD3-expressing clones could be triggered via Tp103 to kill target cells. In contrast, both CD2 and Tp103 pathways were suppressed after modulation of the TCR complex with anti-CD3 mAb. This indicates that the function of Tp103 but not of CD2 is dependent on the expression of a functional Ag receptor on cytotoxic T cells. Furthermore, modulation of the Ag receptor induces a state of unresponsiveness in cytotoxic T cells that cannot be attributed to just the removal of the CD3/TCR complex from the cell membrane.
Fleischer
B
B
Department of Medical Microbiology and Immunology, University of Ulm, FRG.
Sturm
E
E
De Vries
J E
JE
Spits
H
H
D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology; D000954:Antigens, Surface / Q000302:isolation & purification / Q000502:physiology*; D003601:Cytotoxicity Tests, Immunologic; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology*; D008970:Molecular Weight; D010641:Phenotype; D011948:Receptors, Antigen, T-Cell / Q000276:immunology*; D013602:T-Lymphocytes, Cytotoxic / Q000145:classification / Q000276:immunology*; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7
D000945:Antigens, Differentiation, T-Lymphocyte; D000954:Antigens, Surface; D011948:Receptors, Antigen, T-Cell; D018127:Tumor Necrosis Factor Receptor Superfamily, Member 7