Lymphocyte emperipolesis into autologous monocytes in leukocyte cultures exposed to mitogenic lectins

Khavkin, T. N.; Triemer, Richard E.; Yabrov, A.; Küchler, Mirco; Agranovsky, E.

doi:10.1007/bf02899048

Cited by 5 publications

(1 citation statement)

References 22 publications

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“…"inside round about wandering" (10)) and it was observed for the first time by Fischer and Dolschansky in 1929 (7). After that time there have been numerous descriptions of this aspect of lymphocyte behavior occurring with a variety of "host" cells (10,14,15,17,29,31). Ultrastructural characterization of in vitro emperipolesis revealed NK cells (i.e., large granular FcR+ (CD16+) cells) as the emperopoletic cells (2,11,2 1,26).…”

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confidence: 99%

Occurrence and a possible mechanism of penetration of natural killer cells into k562 target cells during the cytotoxic interaction

Radošević¹,

Leeuwen²,

Segers-Nolten³

et al. 1995

Cytometry

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The cytotoxic interaction between cloned human Natural Killer (NK) cells and K562 target cells was studied using confocal laser scanning microscopy (CUM) and conventional fluorescence microscopy. We observed, using fixed as well as living cells, the occurrence of (pseudo)emperipolesis during the interaction. About 30% of conjugated NK cells penetrated, partly or completely, into the target cells (in-conjugation). Virtually all in-conjugated target cells exhibited polymerized actin. Killer cells of inconjugates were frequently seen approaching the target cell nucleus or aligning along it. If the cytotoxic process was inhibited by the absence of calcium neither actin polymerization nor in-conjugation were observed. A kinetic study showed that in-conjugation starts somewhat later than actin polymerization but still within a few minutes after addition of calcium to conjugates previously formed Elucidation of the killing mechanism(s) involved in cell mediated cytotoxic processes has been the subject of numerous studies (6,9,16,23,32). In spite of great efforts of different research groups, the exact cause of target cell death has not been resolved yet. In general, two hypotheses dominate the cytotoxicity literature. According to the "colloid osmosis" mechanism, target cells die due to an osmotic imbalancehhock caused by incorporation of killer cell granule material into the target cell membrane (9,3032). The "internal disintegration" model, on the other hand, implies that interaction with a killer cell activates the self-destroying pathway in the target cell which results in DNA fragmentation and cell death (6,16,23). These two mechanisms, however, need not to be mutually exclusive (33). It is also not clear how much each of them participates in the actual killing processand/or what is the crucial change that ultimately leads to target cell death. It remains to be elucidated whether the changes observed in the target cell during the cytotoxic process, such as pore formation and DNA fragmentation, represent the ultimate cause or simply the consequence of approaching cell death.in the absence of calcium. The presence of cytochalasin D (an inhibitor of actin polymerization) completely inhibited in-conjugation and partly reduced the cytotoxic activity. Zinc ions (endonuclease inhibition) inhibited in-conjugation and decreased the total number of target cells with polymerized actin in a concentration dependent manner. Cytotoxic activity was also reduced but not as efficiently as in-conjugation.Our study demonstrates that in-conjugation represents a significant fraction of the cytotoxic interaction. The results indicate that it may be a consequence of an actin polymerization and endonuclease activity dependent part of a cytotoxic mechanism. o 1995 wi~ey-~iss, ~n c .Key terms: Natural Killer cell, emperipolesis, actin polymerization, endonuclease activity One of the crucial steps during cell mediated cytotoxic interaction is formation of a close contact (conjugate formation) between killer and target cells (1,9,28). The att...

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confidence: 99%

Occurrence and a possible mechanism of penetration of natural killer cells into k562 target cells during the cytotoxic interaction

Radošević¹,

Leeuwen²,

Segers-Nolten³

et al. 1995

Cytometry

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The frequency and significance of megakaryocytic emperipolesis in myeloproliferative and reactive states

Cashell

Buss

1992

Ann Hematol

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Sixty-three bone marrow (BM) biopsy paraffin sections from patients with platelet counts of 1000 x 10(9)/1 or greater were examined to determine the incidence of megakaryocytic emperipolesis for the various myeloproliferative disorders (MPDs) and for reactive thrombocytosis. Of those cases classified as specific MPDs, 77% of primary thrombocythemia (PT) specimens, 100% of the polycythemia vera (PV) specimens, a single idiopathic myelofibrosis (IMF) specimen, and 17% of the chronic granulocytic leukemia (CGL) specimens demonstrated emperipolesis within megakaryocytes. Two of three cases grouped as MPDs but not further classified also demonstrated emperipolesis. Of the cases of reactive thrombocytosis (RT), 75% showed the presence of emperipolesis. Our results indicate that, with the exception of CGL, emperipolesis can be found in the BM megakaryocytes of the great majority of patients who have extreme thrombocytosis. The underlying cause, whether myeloproliferative or reactive, does not apparently influence the incidence of the phenomenon.

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Endocytotic structures and cell processes

Ghadially¹

1988

Ultrastructural Pathology of the Cell and Matrix

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Lymphocyte emperipolesis into autologous monocytes in leukocyte cultures exposed to mitogenic lectins

Cited by 5 publications

References 22 publications

Occurrence and a possible mechanism of penetration of natural killer cells into k562 target cells during the cytotoxic interaction

Occurrence and a possible mechanism of penetration of natural killer cells into k562 target cells during the cytotoxic interaction

The frequency and significance of megakaryocytic emperipolesis in myeloproliferative and reactive states

Endocytotic structures and cell processes

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