Natural killer (NK) cells can spontaneously lyse certain virally infected and transformed cells. However, early in immune responses NK cells are further activated and recruited to tissue sites where they perform effector functions. This process is dependent on cytokines, but it is unclear if it is regulated by NK cell recognition of susceptible target cells. We show here that infiltration of activated NK cells into the peritoneal cavity in response to tumor cells is controlled by the tumor major histocompatibility complex (MHC) class I phenotype. Tumor cells lacking appropriate MHC class I expression induced NK cell infiltration, cytotoxic activation, and induction of transcription of interferon γ in NK cells. The induction of these responses was inhibited by restoration of tumor cell MHC class I expression. The NK cells responding to MHC class I–deficient tumor cells were ∼10 times as active as endogenous NK cells on a per cell basis. Although these effector cells showed a typical NK specificity in that they preferentially killed MHC class I–deficient cells, this specificity was even more distinct during induction of the intraperitoneal response. Observations are discussed in relation to a possible adaptive component of the NK response, i.e., recruitment/activation in response to challenges that only NK cells are able to neutralize.
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3 January 2000
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January 03 2000
Recruitment and Activation of Natural Killer (Nk) Cells in Vivo Determined by the Target Cell Phenotype: An Adaptive Component of Nk Cell–Mediated Responses
Rickard Glas,
Rickard Glas
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
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Lars Franksson,
Lars Franksson
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
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Clas Une,
Clas Une
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
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Maija-Leena Eloranta,
Maija-Leena Eloranta
bDepartment of Veterinary Microbiology, Swedish University of Agricultural Sciences, S-75007 Uppsala, Sweden
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Claes Öhlén,
Claes Öhlén
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
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Anders Örn,
Anders Örn
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
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Klas Kärre
Klas Kärre
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
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Rickard Glas
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
Lars Franksson
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
Clas Une
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
Maija-Leena Eloranta
bDepartment of Veterinary Microbiology, Swedish University of Agricultural Sciences, S-75007 Uppsala, Sweden
Claes Öhlén
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
Anders Örn
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
Klas Kärre
aMicrobiology and Tumor Biology Center, Karolinska Institute, S-171 77 Stockholm, Sweden
Abbreviations used in this paper: DELFIA, dissociation-enhanced lanthanide fluoroimmunoassays; FSC, forward scatter; PECs, peritoneal exudate cells; SSC, side scatter; TAP, transporter associated with antigen processing.
Received:
June 07 1999
Revision Requested:
September 10 1999
Accepted:
September 14 1999
Online ISSN: 1540-9538
Print ISSN: 0022-1007
© 2000 The Rockefeller University Press
2000
The Rockefeller University Press
J Exp Med (2000) 191 (1): 129–138.
Article history
Received:
June 07 1999
Revision Requested:
September 10 1999
Accepted:
September 14 1999
Citation
Rickard Glas, Lars Franksson, Clas Une, Maija-Leena Eloranta, Claes Öhlén, Anders Örn, Klas Kärre; Recruitment and Activation of Natural Killer (Nk) Cells in Vivo Determined by the Target Cell Phenotype: An Adaptive Component of Nk Cell–Mediated Responses. J Exp Med 3 January 2000; 191 (1): 129–138. doi: https://doi.org/10.1084/jem.191.1.129
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