TY - JOUR
T1 - Sublytic complement attack protects tumor cells from lytic doses of antibody and complement
AU - Reiter, Yoram
AU - Ciobotarin, Adina
AU - Fishelson, Zvi
PY - 1992/5
Y1 - 1992/5
N2 - Sublytic doses of the membrane attack complex (MAC) of complement are known to exert multiple stimulatory effects on metabolically active cells. Results presented herewith demonstrate that pretreatment of the human leukemic cells K562 and HL‐60 with sublytic doses of antibody and normal human serum protects them from lytic complement concentrations, a phenomenon proposed to be called “complement‐induced protection”. C7‐ and C8‐deficient human sera are ineffective in inducing resistance unless they are reconstituted with purified human C7 and C8, respectively. The complement‐induced protection is inhibitable by actinomycin D and cycloheximide indicating that the increased complement resistance depends on RNA and protein synthesis triggered by the sublytic complement doses. Free extracellular Ca2+ is also required to achieve maximal protection, indicating a role for Ca2+ ions in the cell stimulatory events which culminate in increased complement resistance. Quantitative analysis of bound complement components indicated that similar amounts of C3 and C9 molecules are deposited on “protected” and control cells during complement activation. The “protected” K562 and HL‐60 cells regain sensitivity to lytic MAC doses after about 8 or 3 h, respectively, of culture in growth medium, in the absence or presence of actinomycin D and cycloheximide. The “induced protection” is not species restricted and protection from human complement can be induced in K562 cells by treatment with sublytic doses of antibody and rabbit or guinea pig sera.
AB - Sublytic doses of the membrane attack complex (MAC) of complement are known to exert multiple stimulatory effects on metabolically active cells. Results presented herewith demonstrate that pretreatment of the human leukemic cells K562 and HL‐60 with sublytic doses of antibody and normal human serum protects them from lytic complement concentrations, a phenomenon proposed to be called “complement‐induced protection”. C7‐ and C8‐deficient human sera are ineffective in inducing resistance unless they are reconstituted with purified human C7 and C8, respectively. The complement‐induced protection is inhibitable by actinomycin D and cycloheximide indicating that the increased complement resistance depends on RNA and protein synthesis triggered by the sublytic complement doses. Free extracellular Ca2+ is also required to achieve maximal protection, indicating a role for Ca2+ ions in the cell stimulatory events which culminate in increased complement resistance. Quantitative analysis of bound complement components indicated that similar amounts of C3 and C9 molecules are deposited on “protected” and control cells during complement activation. The “protected” K562 and HL‐60 cells regain sensitivity to lytic MAC doses after about 8 or 3 h, respectively, of culture in growth medium, in the absence or presence of actinomycin D and cycloheximide. The “induced protection” is not species restricted and protection from human complement can be induced in K562 cells by treatment with sublytic doses of antibody and rabbit or guinea pig sera.
UR - http://www.scopus.com/inward/record.url?scp=0026559725&partnerID=8YFLogxK
U2 - 10.1002/eji.1830220515
DO - 10.1002/eji.1830220515
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
AN - SCOPUS:0026559725
SN - 0014-2980
VL - 22
SP - 1207
EP - 1213
JO - European Journal of Immunology
JF - European Journal of Immunology
IS - 5
ER -