PMID- 8394407
OWN - NLM
STAT- MEDLINE
DCOM- 19930913
LR  - 20210105
IS  - 0022-1007 (Print)
IS  - 1540-9538 (Electronic)
IS  - 0022-1007 (Linking)
VI  - 178
IP  - 3
DP  - 1993 Sep 1
TI  - Recognition of virus-infected cells by natural killer cell clones is controlled 
      by polymorphic target cell elements.
PG  - 961-9
AB  - Natural killer (NK) cells provide a first line of defense against viral 
      infections. The mechanisms by which NK cells recognize and eliminate infected 
      cells are still largely unknown. To test whether target cell elements contribute 
      to NK cell recognition of virus-infected cells, human NK cells were cloned from 
      two unrelated donors and assayed for their ability to kill normal autologous or 
      allogeneic cells before and after infection by human herpesvirus 6 (HHV-6), a 
      T-lymphotropic herpesvirus. Of 132 NK clones isolated from donor 1, all displayed 
      strong cytolytic activity against the NK-sensitive cell line K562, none killed 
      uninfected autologous T cells, and 65 (49%) killed autologous T cells infected 
      with HHV-6. A panel of representative NK clones from donors 1 and 2 was tested on 
      targets obtained from four donors. A wide heterogeneity was observed in the 
      specificity of lysis of infected target cells among the NK clones. Some clones 
      killed none, some killed only one, and others killed more than one of the 
      different HHV-6-infected target cells. Killing of infected targets was not due to 
      complete absence of class I molecules because class I surface levels were only 
      partially affected by HHV-6 infection. Thus, target cell recognition is not 
      controlled by the effector NK cell alone, but also by polymorphic elements on the 
      target cell that restrict NK cell recognition. Furthermore, NK clones from 
      different donors display a variable range of specificities in their recognition 
      of infected target cells.
FAU - Malnati, M S
AU  - Malnati MS
AD  - Laboratory of Immunogenetics, National Institute of Allergy and Infectious 
      Diseases, National Institutes of Health, Rockville, Maryland 20852.
FAU - Lusso, P
AU  - Lusso P
FAU - Ciccone, E
AU  - Ciccone E
FAU - Moretta, A
AU  - Moretta A
FAU - Moretta, L
AU  - Moretta L
FAU - Long, E O
AU  - Long EO
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Exp Med
JT  - The Journal of experimental medicine
JID - 2985109R
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Isoantigens)
SB  - IM
MH  - Clone Cells
MH  - Cytotoxicity, Immunologic
MH  - Herpesviridae Infections/*immunology
MH  - Herpesvirus 6, Human/*immunology
MH  - Histocompatibility Antigens Class I/*immunology
MH  - Humans
MH  - In Vitro Techniques
MH  - Isoantigens/immunology
MH  - Killer Cells, Natural/*immunology
MH  - Polymorphism, Genetic
MH  - T-Lymphocytes/*immunology/microbiology
PMC - PMC2191173
EDAT- 1993/09/01 00:00
MHDA- 1993/09/01 00:01
PMCR- 1994/03/01
CRDT- 1993/09/01 00:00
PHST- 1993/09/01 00:00 [pubmed]
PHST- 1993/09/01 00:01 [medline]
PHST- 1993/09/01 00:00 [entrez]
PHST- 1994/03/01 00:00 [pmc-release]
AID - 93353152 [pii]
AID - 10.1084/jem.178.3.961 [doi]
PST - ppublish
SO  - J Exp Med. 1993 Sep 1;178(3):961-9. doi: 10.1084/jem.178.3.961.