Impact of the NK cell receptor LIR-1 (ILT-2/CD85j/LILRB1) on cytotoxicity against multiple myeloma.
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Impact of the NK cell receptor LIR-1 (ILT-2/CD85j/LILRB1) on cytotoxicity against multiple myeloma. / Heidenreich, Silke; Zu Eulenburg, Christine Gräfin; Hildebrandt, York; Stübig, Thomas; Sierich, Heidi; Badbaran, Anita; Eiermann, Thomas; Binder, Thomas; Kröger, Nicolaus.
In: Clin Dev Immunol, Vol. 2012, 2012, p. 652130.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Impact of the NK cell receptor LIR-1 (ILT-2/CD85j/LILRB1) on cytotoxicity against multiple myeloma.
AU - Heidenreich, Silke
AU - Zu Eulenburg, Christine Gräfin
AU - Hildebrandt, York
AU - Stübig, Thomas
AU - Sierich, Heidi
AU - Badbaran, Anita
AU - Eiermann, Thomas
AU - Binder, Thomas
AU - Kröger, Nicolaus
PY - 2012
Y1 - 2012
N2 - The role of different receptors in natural-killer- (NK-) cell-mediated cytotoxicity against multiple myeloma (MM) cells is unknown. We investigated if an enhancement of NK-cell-mediated cytotoxicity against MM could be reached by blocking of the inhibitory leukocyte immunoglobulin-like receptor 1 (LIR-1). Our investigations revealed high levels of LIR-1 expression not only on the NK cell line NK-92, but also on myeloma cells (MOLP-8, RPMI8226) as well as on a lymphoblastoid cell line (LBCL; IM-9). Subsequent cytotoxicity assays were designed to show the isolated effects of LIR-1 blocking on either the effector or the tumor side to rule out receptor-receptor interactions. Although NK-92 was shown to be capable of myeloma cell lysis, inhibition of LIR-1 on NK-92 did not enhance cytotoxicity. Targeting the receptor on MM and LBCL did not also alter NK-92-mediated lysis. We come to the conclusion that LIR-1 alone does not directly influence NK-cell-mediated cytotoxicity against myeloma. To our knowledge, this work provides the first investigation of the inhibitory capability of LIR-1 in NK-92-mediated cytotoxicity against MM and the first functional evaluation of LIR-1 on MM and LBCL.
AB - The role of different receptors in natural-killer- (NK-) cell-mediated cytotoxicity against multiple myeloma (MM) cells is unknown. We investigated if an enhancement of NK-cell-mediated cytotoxicity against MM could be reached by blocking of the inhibitory leukocyte immunoglobulin-like receptor 1 (LIR-1). Our investigations revealed high levels of LIR-1 expression not only on the NK cell line NK-92, but also on myeloma cells (MOLP-8, RPMI8226) as well as on a lymphoblastoid cell line (LBCL; IM-9). Subsequent cytotoxicity assays were designed to show the isolated effects of LIR-1 blocking on either the effector or the tumor side to rule out receptor-receptor interactions. Although NK-92 was shown to be capable of myeloma cell lysis, inhibition of LIR-1 on NK-92 did not enhance cytotoxicity. Targeting the receptor on MM and LBCL did not also alter NK-92-mediated lysis. We come to the conclusion that LIR-1 alone does not directly influence NK-cell-mediated cytotoxicity against myeloma. To our knowledge, this work provides the first investigation of the inhibitory capability of LIR-1 in NK-92-mediated cytotoxicity against MM and the first functional evaluation of LIR-1 on MM and LBCL.
KW - Animals
KW - Humans
KW - COS Cells
KW - Cercopithecus aethiops
KW - Cell Line
KW - Antibodies, Monoclonal/immunology
KW - Antibodies, Blocking/immunology
KW - Antigens, CD/immunology
KW - Cytotoxicity, Immunologic
KW - Killer Cells, Natural/immunology/metabolism
KW - Multiple Myeloma/immunology
KW - Receptors, Immunologic/antagonists & inhibitors/immunology
KW - Animals
KW - Humans
KW - COS Cells
KW - Cercopithecus aethiops
KW - Cell Line
KW - Antibodies, Monoclonal/immunology
KW - Antibodies, Blocking/immunology
KW - Antigens, CD/immunology
KW - Cytotoxicity, Immunologic
KW - Killer Cells, Natural/immunology/metabolism
KW - Multiple Myeloma/immunology
KW - Receptors, Immunologic/antagonists & inhibitors/immunology
U2 - 10.1155/2012/652130
DO - 10.1155/2012/652130
M3 - SCORING: Journal article
VL - 2012
SP - 652130
ER -
