CD4 but not CD8 is comodulated with the T-cell antigen receptor (TCR) after activation of a CD4+ CD8+ human leukemia line with staphylococcal enterotoxin

• Published in: Immunology letters Vol. 37; no. 1; p. 53
• Main Authors: Bodó, I, Vloka, J D, Cleveland, W L
• Format: Journal Article
• Language: English
• Published: Netherlands 01-07-1993
• Subjects: Antibodies, Monoclonal - immunology; Antigens, Surface - immunology; CD3 Complex - immunology; CD4-Positive T-Lymphocytes - immunology; Enterotoxins - immunology; Humans; Interleukin-2 - biosynthesis; Lymphocyte Activation - immunology; Mitogens - immunology; Receptors, Antigen, T-Cell, alpha-beta - immunology; T-Lymphocytes - immunology; T-Lymphocytes, Regulatory - immunology; Tetrazolium Salts; Thiazoles; Tumor Cells, Cultured
• DOI: 10.1016/0165-2478(93)90132-L
• ISSN: 0165-2478

Recent studies support the possibility of an interaction between CD4/8 and the TCR complex. To determine if there is specificity in this interaction, we have studied the comodulation of CD4/8 with the CD3/TCR complex on a CD4+ CD8+ human leukemic T-cell line stimulated with staphylococcal enterotoxin A (SEA) bound to Raji cells. FACS analysis revealed that CD3 and the TCR were modulated from the surface. CD4 and not CD8 was comodulated with the T-cell receptor complex, supporting the existence of a docking site on the TCR with selectivity for CD4 or CD8 but not both. Fewer than 45 SEA molecules per presenting cell led to detectable comodulation. The ratio of %CD4/%TCR modulation varied with both time and the amount of SEA used for stimulation. ConA or PHA induced modulation of CD3 but, unlike SEA, failed to induce IL-2 secretion, suggesting multiple pathways and states of T-cell activation. Our findings also suggest that some human T leukemic lines can respond to antigen.