Murine Natural Killer Cells and Hybrid Resistance to Hemopoietic Cells In Vivo

Liu, Jingxuan; George, Thaddeus C.; Devora, Gene A.; Sivakumar, Pallavur V.; Davenport, Colleen; Lai, Wayne C.; Schatzle, John D.; Kumar, Vinay; Bennett, Michael V. L.

doi:10.1385/1-59259-044-6:61

Cited by 4 publications

(8 citation statements)

References 2 publications

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“…Effector phase of NK cells are regulated by inhibitory and activating receptors. Each NK cell is known to express one or more inhibitory receptors, which interact with specific MHC class I molecules on the target cells(Liu et al , 2000). Interaction of MHC class I with the inhibitory Ly49 receptors prevent the activation of NK cells and thereby the lysis of the target cell.…”

Section: Introductionmentioning

confidence: 99%

Murine NKG2D ligands: “Double, double toil and trouble”

Samarakoon

Chu

Malarkannan

2009

Molecular Immunology

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Section: Introductionmentioning

confidence: 99%

Murine NKG2D ligands: “Double, double toil and trouble”

Samarakoon

Chu

Malarkannan

2009

Molecular Immunology

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“…Second, the donor cells must avoid rejection by the recipient immune system. We and others have shown that natural killer (NK) cells may function early after transplant, to reduce the effective stem cell innoculum that is available for engraftment (1–11). This NK effect may become clinically significant during BMT with limited donor cells (such as with umbilical cord blood transplants for hematologic disease (12–14)), or with deceased donor transplants (as could be envisioned with potentially tolerogenic combined bone marrow and solid organ transplantation).…”

Section: Introductionmentioning

confidence: 99%

“…That NK cells can recognize and eliminate donor bone marrow has been shown rigorously in rodents (1–11), and by inference in nonhuman primate experiments (15) and in clinical transplantation (16,17). This recognition relies on signaling through both inhibitory and activating receptors.…”

Section: Introductionmentioning

confidence: 99%

NK Cells Rapidly Reject Allogeneic Bone Marrow in the Spleen Through a Perforin‐ and Ly49D‐Dependent, but NKG2D‐Independent Mechanism

Hamby

Trexler

Pearson

et al. 2007

American Journal of Transplantation

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We have used a sensitive and specific in vivo killing assay to monitor the kinetics, anatomic location and mechanisms controlling NK-mediated rejection of Balb/c bone marrow by C57BL/6 natural killer (NK) cells. We find that NK killing of fully allogeneic bone marrow is a rapid, highly efficient process, leading to substantial rejection of transplanted marrow within 6 h of transplant and elimination of 85% of the transplanted cells within 2 days. NK-mediated rejection occurred predominantly in the spleen, with sparing of rejection in the bone marrow and lymph nodes. Rejection was dependent on Perforin gene function, but was independent of interferon-gamma. Finally, rejection of Balb/c bone marrow by B6 NK cells required signaling through the Ly49D receptor, but occurred despite blockade of NKG2D, which distinguishes these results from previous studies using semiallogeneic transplant pairs. These results identify NK cells as highly active mediators of bone marrow rejection, and suggest that inhibiting NK function early during transplantation may increase the efficiency of engraftment and allow successful engraftment of limiting doses of donor bone marrow.

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“…Each NK cell is known to express one or more inhibitory receptors, which interact with a specific MHC class I molecules on the target cells [14]. Interaction of MHC class I with the Ly49 receptors prevent the activation of NK cells and thereby the lysis of the target cell.…”

Section: Introductionmentioning

confidence: 99%

The balancing act: Inhibitory Ly49 regulate NKG2D-mediated NK cell functions

Malarkannan

2006

Seminars in Immunology

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NK cells use NKG2D receptor to recognize 'induced-self'. In apparent violation of the 'missingself' hypothesis, NK cells stimulated through NKG2D can lyse target cells despite normal expression levels of MHC class I molecules. Although, 'overriding' of the inhibitory by the activating signals had been postulated the precise role of inhibitory Ly49 receptors on NKG2D-mediated activation has only started emerging. We propose that NKG2D-mediated activation is a function of 'altering the balance' in the signaling strength between the activating NKG2D and inhibiting Ly49 receptors. Balance in the signaling strength depends on the expression levels of activating ligands on the target cells. Qualitative and quantitative variations of MHC class I molecules expressed on the target cells also plays a major role in determining this 'altered-balance'. Consequently, the nature of Ly49 receptors expressed on specific NK subsets determines the level of NKG2D-mediated NK cell activation. These observations provide a firm basis of 'altered-balance' in NK signaling and describe an active interplay between inhibitory Ly49 and activating NKG2D receptors.

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Murine Natural Killer Cells and Hybrid Resistance to Hemopoietic Cells In Vivo

Cited by 4 publications

References 2 publications

Murine NKG2D ligands: “Double, double toil and trouble”

Murine NKG2D ligands: “Double, double toil and trouble”

NK Cells Rapidly Reject Allogeneic Bone Marrow in the Spleen Through a Perforin‐ and Ly49D‐Dependent, but NKG2D‐Independent Mechanism

The balancing act: Inhibitory Ly49 regulate NKG2D-mediated NK cell functions

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