A patient with simultaneous absence of “classical” natural killer cells (CD3−, CD16+, and NKH1+) and expansion of CD3+, CD4−, CD8−, NKH1+ subset

Ballas, Zuhair K.; Turner, James M. A.; Turner, Deborah; Goetzman, Elizabeth A.; Kemp, John D.

doi:10.1016/0091-6749(90)90155-w

Cited by 65 publications

(39 citation statements)

References 27 publications

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“…[39][40][41] While rare, these patients suffer from recurrent viral infections, suggesting that other unrecognized patients may have succumbed to infection. Regardless, the molecular basis for these clinical disorders is currently unknown.…”

Section: Org Frommentioning

confidence: 99%

Arrested natural killer cell development associated with transgene insertion into the Atf2 locus

Kim

Song

Higuchi

et al. 2006

Blood

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IntroductionNatural killer (NK) cells constitute the third major population of lymphocytes and play critical roles in innate immune responses to pathogens and tumors. 1 They can be distinguished from other lymphocytes by their lack of B-or T-cell antigen receptor expression. Indeed, NK-cell development is independent of events required for B-and T-cell antigen receptor gene rearrangement, as illustrated by normal NK cells found in mice with defects in the recombination machinery, such as scid, and Rag-deficiency. However, NK-cell developmental pathways are just beginning to be elucidated (reviewed in Yokoyama et al 2 and Colucci et al 3 ).NK cells appear to develop completely in the bone marrow (BM). Based on the differential expression of cell-surface markers and NK-cell functional assays, we previously proposed a developmental model of mouse NK cells. 4 Cells at putative developmental stages can be distinguished from each other and from cells resembling mature peripheral NK cells. The earliest detectable precursor committed to the NK-cell lineage (stage 1) expresses CD122 (IL-2/IL-15R␤) 5-7 that is then expressed throughout NKcell maturation. Although this receptor subunit is associated with the interleukin-2 receptor (IL-2R) complex, its contribution to the IL-15R complex is probably the most relevant for NK-cell development because mice deficient in IL-15 or IL-15R␣ completely lack NK cells with relative preservation of the development of other lymphocytes. 8,9 Developing NK cells express NK1.1 (NKR-P1C) (stages 2 to 5), consistent with studies of in vitro development of human NK cells, indicating that the NKR-P1A molecule is one of the earliest markers expressed. 10 Among the NK1.1 ϩ CD122 ϩ population, there is an ␣v integrin ϩ c-kit Ϫ population (stage 2) that expresses the CD94/NKG2 receptor without concomitant expression of Ly49 receptors. This is also consistent with observations that CD94/NKG2 receptors are found on fetal or neonatal NK cells without Ly49 receptor expression. 11,12 Subsequently, the NK1.1 ϩ cells express Ly49 receptors, and also c-kit and ␣v (stage 3). When ␣v expression then decreases, ␣2 integrin (DX5) expression increases (stage 4). At this stage, developing NK cells undergo constitutive proliferation in the BM. Subsequently, as NK cells finally acquire expression of Mac-1 and CD43 at levels comparable to peripheral NK cells (stage 5), NK-cell proliferation wanes. Concomitant with high-level expression of Mac-1 and CD43, there is full functional maturation of NK cells with development of cytotoxicity and cytokine production that closely resembles mature, peripheral NK cells. Thus, NK cells, like other hematopoietic cells, undergo a series of developmental steps in order to become fully mature, though the molecular basis for these stages remains to be determined.Analysis of targeted mutant and transgenic mice has revealed factors and precursor cells that contribute to NK-cell development, but most of these factors affect NK-cell development at stages For personal use only. on May 10...

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Section: Org Frommentioning

confidence: 99%

Arrested natural killer cell development associated with transgene insertion into the Atf2 locus

Kim

Song

Higuchi

et al. 2006

Blood

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“…People with severe NK cell deficiency suffer from increased infections and may be susceptible to certain tumors (Ballas et al, 1990;Biron et al, 1989). Aging also is associated with risk of serious infection and cancer (Pawelec et al, 2003), so it is appropriate to question whether NK cell function is impaired in aging.…”

Section: Introductionmentioning

confidence: 99%

Reciprocal age related change in natural killer cell receptors for MHC class I

Lütz

Moore

Bradley

et al. 2005

Mechanisms of Ageing and Development

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Natural killer (NK) cells are essential for healthy aging. NK cell activation is controlled by MHC class I-specific CD94/NKG2 receptors and killer immunoglobulin-like receptors (KIR). To assess NK cytotoxic function in isolation from MHC receptor engagement, we measured the ability of purified NK cells to kill mouse P815 target cells in the presence of anti-CD16 mAb. CD16-mediated cytotoxicity did not change with age, indicating that NK activation and cytotoxic granule release remained functional. We then investigated MHC class I receptor expression on NK cells. There was an age related decrease in CD94 and NKG2A expression and a reciprocal age related increase in KIR expression. NKG2A expression also declined with age on CD56 + T cells. CD94/ NKG2A receptor function was proportional to expression, indicating that NK cell inhibitory signaling pathways were intact. NKG2A and KIR expression were complementary, suggesting that CD94/NKG2A function could substitute for inhibitory KIR function during polyclonal NK cell development in both young and elderly adults. The distinct roles of CD94/NKG2A and KIR receptors suggest that shifting MHC class I receptor expression patterns reflect age related changes in NK cell and CD56 + T cell turnover and function in vivo.

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“…N atural killer cells constitute a subset of lymphocytes that contributes to the innate immune response against intracellular pathogens (1,2) and may mediate tumor surveillance (3). Unlike B cells, which produce Abs, NK cells use effector mechanisms similar to those of T cells.…”

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confidence: 99%

Costimulation of Multiple NK Cell Activation Receptors by NKG2D

Carayannopoulos

Poursine-Laurent

et al. 2002

The Journal of Immunology

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The activation of NK cells is mediated through specific interactions between activation receptors and their respective ligands. Little is known, however, about whether costimulation, which has been well characterized for T cell activation, occurs in NK cells. To study the function of NKG2D, a potential NK costimulatory receptor, we have generated two novel hamster mAbs that recognize mouse NKG2D. FACS analyses demonstrate that mouse NKG2D is expressed on all C57BL/6 IL-2-activated NK (lymphokine-activated killer (LAK)) cells, all splenic and liver NK cells, and ∼50% of splenic NKT cells. Consistent with limited polymorphism of NKG2D, its sequence is highly conserved, and the anti-NKG2D mAbs react with NK cells from a large number of different mouse strains. In chromium release assays, we show that stimulation of NK cells with anti-NKG2D mAb can redirect lysis. Also, enhanced lysis of transfected tumor targets expressing NKG2D ligand could be inhibited by addition of anti-NKG2D mAb. Interestingly, stimulation of LAK cells via NKG2D alone does not lead to cytokine release. However, stimulation of LAK via both an NK activation receptor (e.g., CD16, NK1.1, or Ly-49D) and NKG2D leads to augmentation of cytokine release compared with stimulation through the activation receptor alone. These results demonstrate that NKG2D has the ability to costimulate multiple NK activation receptors.

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A patient with simultaneous absence of “classical” natural killer cells (CD3−, CD16+, and NKH1+) and expansion of CD3+, CD4−, CD8−, NKH1+ subset

Cited by 65 publications

References 27 publications

Arrested natural killer cell development associated with transgene insertion into the Atf2 locus

Arrested natural killer cell development associated with transgene insertion into the Atf2 locus

Reciprocal age related change in natural killer cell receptors for MHC class I

Costimulation of Multiple NK Cell Activation Receptors by NKG2D

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