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Four monoclonal antibodies VEP8, VEP9, VIM-D5, VIB-C5 against antigens expressed on human mature myeloid cells (polymorphonuclear leukocytes [PMNL] and/or monocytes) as well as on immature cells in the bone marrow were tested for reactivity with cell preparations highly enriched for large granular lymphocytes (LGL). These cells are known to be the main effector cells responsible for natural killer (NK) cell activity in human peripheral blood. Using indirect membrane immunofluorescence (IMF), none of these antibodies showed any reactivity at all. In addition, LGL-enriched cell preparations were tested with the anti-lymphocyte monoclonal antibodies OKT6, anti-Leu1, anti-Leu2a, anti-Leu3a, and anti-human Lyt3, and also with OKM1 antibody. Significant reactivity was found with anti-Leu2a (59 +/- 8%), anti-Lyt3 (55 +/- 4%) and OKM1 (81 +/- 11%) antibodies, whereas T6, Leu1, and Leu3a antigens were less pronounced or missing on LGL. As a further approach, another monoclonal antibody, VEP13, which reacts with LGL, granulocytes but not monocytes and is therefore different in its specificity from OKM1 and OKT10, was used for identification of LGL. The coexpression of antigens as defined by the above-mentioned antibodies and OKT10 on VEP13+ cells was studied. Again, phenotypes similar to those observed on LGL enriched by Percoll gradient centrifugation were found: of VEP13+ cells 84 +/- 6% reacted with OKM1, 82 +/- 5% with OKT10, 52 +/- 17% with anti-human Lyt3, and 48 +/- 14% with anti-Leu2a, whereas VEP8, VEP9, VIM-D5, VIB-C5, T6, Leu1, Leu3a antigens were not expressed on VEP13+ cells. Taken together as an overall evaluation of phenotypic characteristics, our data indicate that LGL cannot be integrated into one of the known lymphocytic or myelomonocytic lineages. LGL show an intermediate phenotype depending possibly on varying differentiation or activation stages of haemopoietic cells. However, the possibility also exists that LGL belong to a separate, yet undefined cell lineage.
H Rumpold, and
D Kraft, and
G Obexer, and
T Radaszkiewicz, and
O Majdic, and
P Bettelheim, and
W Knapp, and
G Böck
February 1988,
Immunology,
H Rumpold, and
D Kraft, and
G Obexer, and
T Radaszkiewicz, and
O Majdic, and
P Bettelheim, and
W Knapp, and
G Böck
September 1985,
Blood,
H Rumpold, and
D Kraft, and
G Obexer, and
T Radaszkiewicz, and
O Majdic, and
P Bettelheim, and
W Knapp, and
G Böck
June 1986,
Acta pathologica, microbiologica, et immunologica Scandinavica. Section B, Microbiology,
H Rumpold, and
D Kraft, and
G Obexer, and
T Radaszkiewicz, and
O Majdic, and
P Bettelheim, and
W Knapp, and
G Böck
April 1987,
Cellular immunology,
H Rumpold, and
D Kraft, and
G Obexer, and
T Radaszkiewicz, and
O Majdic, and
P Bettelheim, and
W Knapp, and
G Böck
March 1985,
Blood,
H Rumpold, and
D Kraft, and
G Obexer, and
T Radaszkiewicz, and
O Majdic, and
P Bettelheim, and
W Knapp, and
G Böck
January 1981,
Immunological reviews,
H Rumpold, and
D Kraft, and
G Obexer, and
T Radaszkiewicz, and
O Majdic, and
P Bettelheim, and
W Knapp, and
G Böck
January 1985,
Proceedings of the National Academy of Sciences of the United States of America,
H Rumpold, and
D Kraft, and
G Obexer, and
T Radaszkiewicz, and
O Majdic, and
P Bettelheim, and
W Knapp, and
G Böck
May 1987,
Journal of immunology (Baltimore, Md. : 1950),
H Rumpold, and
D Kraft, and
G Obexer, and
T Radaszkiewicz, and
O Majdic, and
P Bettelheim, and
W Knapp, and
G Böck
April 1986,
International journal of cancer,
H Rumpold, and
D Kraft, and
G Obexer, and
T Radaszkiewicz, and
O Majdic, and
P Bettelheim, and
W Knapp, and
G Böck
March 1988,
The Tohoku journal of experimental medicine,
