title: Apoptotic cells actively inhibit the expression of CD69 on Con A activated T lymphocytes.
abstract: Although apoptosis is commonly viewed as a silent cell death without damage to adjacent tissues, the effect of apoptosis on immunity has been unclear. We have investigated the influence of apoptotic cells on T-cell activation. The K562 or HL-60 human leukemia cell lines that had been induced apoptosis by FTY720 or cycloheximide (CHX) were added into the culture of mouse spleen cells stimulated with Con A. Six to 20 h later, the expression of CD69, an early T-cell activation antigen, was detected using flowcytometry. Living cells and necrotic cells served as control groups. Apoptotic K562 or HL-60 cells induced by either FTY720 or CHX unanimously inhibited CD69 expression on the CD3+ mouse T cells while living and necrotic cells did not. The inhibition was proportional to the number of apoptotic cells and was different in the T-cell subsets, showing a rapid and transient inhibition on the CD3+CD8+ T-cell activation but with a slow and continuous inhibition on CD3+CD8- T-cell activation. In conclusion, the apoptotic cells actively inhibit a T-cell activation that is independent of the cell lines or the apoptotic inducers, indicating that the apoptotic cells dominantly regulate T-cell immunity.
authors.affiliation: Hemopurification and Renal Transplantation Center, Zhujiang Hospital, Guangzhou, China.
authors.forename: E
authors.initials: E
authors.lastname: Sun
authors.forename: L
authors.initials: L
authors.lastname: Zhang
authors.forename: Y
authors.initials: Y
authors.lastname: Zeng
authors.forename: Q
authors.initials: Q
authors.lastname: Ge
authors.forename: M
authors.initials: M
authors.lastname: Zhao
authors.forename: W
authors.initials: W
authors.lastname: Gao
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis* / Q000276:immunology; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis* / Q000276:immunology; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology*; D003208:Concanavalin A / Q000494:pharmacology*; D003513:Cycloheximide / Q000494:pharmacology; D004306:Dose-Response Relationship, Immunologic; D000068876:Fingolimod Hydrochloride; D018922:HL-60 Cells; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology; D020014:K562 Cells; D037181:Lectins, C-Type; D007958:Leukocyte Count; D008213:Lymphocyte Activation / Q000187:drug effects / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D011409:Propylene Glycols / Q000494:pharmacology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D013110:Sphingosine / Q000031:analogs & derivatives; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism*; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D003208:Concanavalin A; D003513:Cycloheximide; D000068876:Fingolimod Hydrochloride; D007166:Immunosuppressive Agents; D037181:Lectins, C-Type; D011409:Propylene Glycols; D011500:Protein Synthesis Inhibitors; D013110:Sphingosine; D000099192:CD69 Antigens