Divergent and convergent evolution of NK-cell receptors

Barten, Roland; Torkar, Michaela; Haude, Anja; Trowsdale, John; Wilson, Michael J.

doi:10.1016/s1471-4906(00)01802-0

Cited by 139 publications

(123 citation statements)

References 55 publications

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“…Despite competition with excessive ILT4 position 1 nucleotides, significant amounts of Sp1 family proteins were still bound to the ILT2 position 1 probe, as shown by supershifts with anti-Sp1, anti-Sp3, or both (left columns, lanes 8 -10) and competition with Sp1 consensus oligos (lane 11). In contrast, ILT4 position 1 probe did not show any binding of Sp1 family proteins in competition with ILT2 position 1 nucleotides (right columns, lanes [7][8][9][10][11][12]. These findings suggest that the affinity of ILT2 position 1 to Sp1 family proteins was much higher than that of ILT4 position 1.…”

Section: Nuclear Factors Involved In Ilt2/4 Trans-activationmentioning

confidence: 83%

“…In addition, ILT2 binds to the viral class I-like molecule UL-18 encoded by human CMV (HCMV) (6). Genetically, functionally, and structurally, the ILT family is closely related to the KIR family, also mapped to leukocyte receptor complex (7)(8)(9)(10)). An outstanding property of ILTs is their cellular distribution, which greatly differs from that of KIRs expressed on NK cells and some T cells.…”

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confidence: 99%

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Transcriptional Regulation of ILT Family Receptors

Nakajima

Asai

Okada

et al. 2003

The Journal of Immunology

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Ig-like transcripts (ILT/leukocyte Ig-like receptor/monocyte/macrophage Ig-like receptor or CD85) are encoded on human chromosome 19q13.4, designated the human leukocyte receptor complex, and are predominantly expressed on myeloid lineage cells. We investigated the transcriptional regulation of ILT1, ILT2, and ILT4 genes to elucidate control mechanisms operating on the specific expression of ILT receptors. Inhibitory ILT2 and ILT4 both have a similar genomic structure, in which the ∼160-bp 5′-flanking regions function as core promoters with critically important PU.1 binding sites. However, an Sp1 family-binding GC-box is more influential in trans-activation of ILT2 than ILT4. Additionally, ILT4 transcription is tightly regulated by chromatin modifications accompanied by histone acetylation, which strictly controls expression within myeloid lineage cells. Activating ILT1 carries a core promoter corresponding to the intronic region of ILT2 and ILT4, where PU.1 and Runx1 binding sites are essential, but a downstream heat shock element also augments promoter activity. Thus, each ILT is regulated by a distinct transcriptional mechanism, although PU.1 acts as a common trans-acting factor. We also found that human CMV infection strongly trans-activates inhibitory ILT2 and ILT4 genes through the expression of immediate-early proteins.

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Section: Nuclear Factors Involved In Ilt2/4 Trans-activationmentioning

confidence: 83%

mentioning

confidence: 99%

Transcriptional Regulation of ILT Family Receptors

Nakajima

Asai

Okada

et al. 2003

The Journal of Immunology

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“…We note with interest that the Haymaker gene is located on chromosome 19 within a cluster of a number of families of NK cell receptors at 19q13.1 to 19q13.4. 33,34 .…”

Section: Semiquantitative Analysis Of P385 Gene Transcriptionmentioning

confidence: 99%

Genetic identity and differential expression of p38.5 (Haymaker) in human malignant and nonmalignant cells

et al. 2001

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Previous studies from our laboratory revealed a novel protein of 38.5 kD on the surface of malignant cell lines of hematopoetic origin that exhibit susceptibility to naive natural killer (NK) cell-mediated lysis. In contrast, p38.5 was not detected on the surface of NK cell-resistant carcinoma cell lines or normal cells. We now report that this protein is differentially expressed, intracellularly, in malignant cell lines of both hematopoetic and epithelial origin compared with nonmalignant cells. To characterize p38.5 further, we used a previously developed antipeptide antibody (anti-11-mer) to probe cDNA expression libraries and subsequently per-

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“…97 In humans, the family of killer cell immunoglobulinlike receptors (KIR) are considered the functional homologues of mouse Ly49 proteins. 98 KIR receptors are specific for various MHC class I molecules, they are expressed in overlapping subsets of NK cells, and include inhibitory or activating members that signal through the same intracellular pathways as Ly49 molecules. KIR genes are localized to chromosome 19q13 in a region known as the leukocyte receptor cluster (LRC) (Figure 1b).…”

Section: Mouse Models Of CMV Infectionmentioning

confidence: 99%

“…KIR genes are localized to chromosome 19q13 in a region known as the leukocyte receptor cluster (LRC) (Figure 1b). 98,99 This region also encodes other members of the immunoglobulin superfamily such as the immunoglobulin-like transcrips (ILTs) and the leukocyte-associated inhibitory receptor (LAIRs) that are expressed on an extended range of cell types, as well as NKp46, an activating NK receptor. Whereas Nkp46 and the gene cluster of paired-immunoglobulin like receptor family (Pir), likely orthologous of ILTs, are localized to a syntenic region on mouse chromosome 7, KIRs are completely absent from rodents ( Figure 1b).…”

Section: Mouse Models Of CMV Infectionmentioning

confidence: 99%

Genetic control of innate immune responses against cytomegalovirus: MCMV meets its match

2002

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Cytomegalovirus (CMV) is a widespread pathogen that is All Ly49 receptors characterized to date interact with MHC class I molecules on potential target cells, resulting in the accumulation of signals to the NK to either 'kill' or 'ignore' the cell based upon the repertoire of MHC class I molecules expressed. The identification of Cmv1 as Ly49H, a stimulatory member of the Ly49 family, adds an interesting twist to the Ly49 story. Although the ligand of Ly49H is not yet known, there is already compelling evidence that the ligand is upregulated on virally infected cells, resulting in specific activation of Ly49H-expressing NK cells. This review provides an historical perspective of the MCMV infection model from its inception to the discovery of the gene responsible for the phenotype and provides a basis for further experiments aimed at understanding the role of NK cells, in general, and Ly49H, in particular, in mediating resistance to cytomegalovirus.

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Divergent and convergent evolution of NK-cell receptors

Cited by 139 publications

References 55 publications

Transcriptional Regulation of ILT Family Receptors

Transcriptional Regulation of ILT Family Receptors

Genetic identity and differential expression of p38.5 (Haymaker) in human malignant and nonmalignant cells

Genetic control of innate immune responses against cytomegalovirus: MCMV meets its match

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