Specificity, Function, and Development of NK Cells: NK by L. L. Wang, W. M. Yokoyama (auth.), Dr. Klas Kärre, Marco

By L. L. Wang, W. M. Yokoyama (auth.), Dr. Klas Kärre, Marco Colonna M.D. (eds.)

Our realizing of the functionality of common killer (NK) cells has dramatically replaced in recent times. the invention of NK receptors particular for MHC classification I molecules, and the research of the function of co-stimulatory and adhesion molecules have ended in an knowing of ways NK cells realize tumor and virally contaminated cells that experience misplaced expression of MHC type I molecules or have altered distribution of ordinary phone floor molecules. Such attractiveness occasions result in intracellular signs that are both stimulatory or inhibitory. This booklet offers an perception into how NK cells strengthen, how they discover ways to distinguish altered cells from basic cells, and into their organic function in controlling infections and tumors.

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The signaling properties of NKG2-A and NKG2-C cytoplasmic domains coupled to murine NKR-Pl extracellular region have been recently reported (HOUCHINS et ai. 1997). By reverse-transcriptase polymerase chain reaction analysis in a limited number of NK clones we have confirmed that Z199+ group B cells express NKG2-A and p39+ group A cells express NKG2-CIE. However, several NKG2 sequences are amplified in some clones, further suggesting that the expression of the various CD94INKG2 dimers is not mutually exclusive (PEREZ-VILLAR et ai.

1997). On the other hand, CTL recognize foreign antigens using a T cell antigen receptor (TcR); however, T cells require time to undergo clonal expansion after exposure to pathogens, but once generated these effectors are able to act with precision to eliminate infected cells and provide long-term specific immunity (reviewed in ZINKERNAGEL et al. 1996). 3 The Central Role ofMHC Class I Molecules in CTL and NK Cell Responses MHC class I molecules are expressed on the surface of most nucleated cells and are composed of a polymorphic heavy chain, a nonpolymorphic light chain (P2-microglobulin, P2m) and a variable peptide of eight to ten amino acids (reviewed in YORK and ROCK 1996).

Fig. 1. Structure of the CD94INKG2 C-type lectin receptor complex are homologous to NKG2-A but lack cytoplasmic ITIMs (Fig. 2); consequently, the CD94INKG2-C and CD94INKG2-E dimers are not expected to exert an inhibitory function and likely correspond to the activating receptors (CD94/p39; Fig. 1). The signaling properties of NKG2-A and NKG2-C cytoplasmic domains coupled to murine NKR-Pl extracellular region have been recently reported (HOUCHINS et ai. 1997). By reverse-transcriptase polymerase chain reaction analysis in a limited number of NK clones we have confirmed that Z199+ group B cells express NKG2-A and p39+ group A cells express NKG2-CIE.

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