IL-4 induces LFA-1 and LFA-3 expression on Burkitt's lymphoma cell lines. Requirement of additional activation by phorbol myristate acetate for induction of homotypic cell adhesions.
LFA-1 and LFA-3 expression is absent or low on Burkitt's lymphoma cell lines and low on the EBV-transformed B cell line UD61. Incubation of cells of BL2 and of UD61 with various concentrations of IL-4 resulted in induction of LFA-1 and LFA-3 expression in a dose dependent fashion. This effect was already observed after 16 h of incubation whereas maximal expression was obtained after 72 h. Induction of LFA-1 and LFA-3 expression seemed to be specific for IL-4, because IL-1, IL-2, IL-3, IFN-alpha, IFN-gamma and a low m.w. B cell growth factor were ineffective. LFA-1 and LFA-3 induction by IL-4 was blocked specifically by an anti-IL-4 antiserum. Induction of LFA-1 expression by IL-4 was furthermore confirmed at the specific LFA-1 beta-chain mRNA level. IL-4 was unable to induce LFA-1 expression on EBV-transformed lymphoblastoid cell lines of two LFA-1-deficient patients. BL2 grows as single cells, but induction of LFA-1 and LFA-3 expression by IL-4 was insufficient to induce homotypic cell adhesions and required PMA as a second signal. PMA alone did not induce LFA-1 antigen expression and was unable to induce adhesions between BL2 cells in the absence of IL-4 in 22 h assays. Addition of PMA to BL2 cells that expressed LFA-1 Ag upon incubation with IL-4 resulted in aggregate formation within 30 min. Adhesions between BL2 cells induced by IL-4 in combination with PMA were blocked by anti-LFA-1 beta or anti-LFA-1 alpha-chains mAb. In addition, these mAbs dispersed preformed aggregates of BL2 cells. Our results indicate that IL-4 can induce the adhesion molecules LFA-1 and LFA-3 on B cell lines, but that an additional activation signal provided by PMA was required for the induction of homotypic cell adhesions.
Rousset
F
F
UNICET, Laboratory for Immunological Research, Dardilly, France.
Billaud
M
M
Blanchard
D
D
Figdor
C
C
Lenoir
G M
GM
Spits
H
H
De Vries
J E
JE
D000911:Antibodies, Monoclonal / Q000502:physiology; D000943:Antigens, Differentiation / Q000096:biosynthesis* / Q000276:immunology; D000954:Antigens, Surface / Q000172:deficiency; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D001667:Binding, Competitive; D002051:Burkitt Lymphoma / Q000276:immunology* / Q000473:pathology; D002448:Cell Adhesion / Q000187:drug effects; D015815:Cell Adhesion Molecules; D002449:Cell Aggregation / Q000187:drug effects; D002461:Cell Line, Transformed; D004306:Dose-Response Relationship, Immunologic; D004854:Herpesvirus 4, Human / Q000276:immunology; D006801:Humans; D015847:Interleukin-4; D007378:Interleukins / Q000494:pharmacology*; D007700:Kinetics; D008213:Lymphocyte Activation; D016169:Lymphocyte Function-Associated Antigen-1; D012333:RNA, Messenger / Q000378:metabolism; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*; D014158:Transcription, Genetic
D000911:Antibodies, Monoclonal; D000943:Antigens, Differentiation; D000954:Antigens, Surface; D015815:Cell Adhesion Molecules; D007378:Interleukins; D016169:Lymphocyte Function-Associated Antigen-1; D012333:RNA, Messenger; D015847:Interleukin-4; D013755:Tetradecanoylphorbol Acetate