ライフサイエンスコーパス: missing self

1 lass I ligands in the mismatched recipient ("missing self").

2 hough NK cells can be held in check against "missing self," acute inflammation driven by infection ca

3 This "missing self" alloresponse to C2, however, is rarely obs

4 target cell recognition by NK cells beyond "missing self" and "induced self," mediated through a tum

5 These data support the "missing self" and not the "hemopoietic histocompatibilit

6 ised rejection of allogeneic, xenogeneic and missing self bone-marrow grafts.

7 veal that splenic DCs survey blood cells for missing self-CD47, a process that might contribute to de

8 HLA-C2, indicating that neither nonself nor missing-self discrimination was operative.

9 at NK cells provide immune surveillance for "missing self," e.g., they eliminate cells that have lost

10 This conclusion is consistent with the missing self hypothesis of NK cell reactivity, and is in

11 Karre et al. later proposed 'the missing self hypothesis' to explain the mechanism by whi

12 f class I molecules was not predicted by the missing self hypothesis.

13 According to the missing-self hypothesis, natural killer (NK) cells surve

14 These results extend the "missing self" hypothesis to suggest that NK Ly49 inhibit

15 This is consistent with the "missing self" hypothesis, which postulates that NK cells

16 o longer express class I MHC molecules (the 'missing self' hypothesis).

17 Thus, these findings broaden the 'missing-self' hypothesis from solely involving MHC class

18 receptors leads to loss of MHC-I-dependent "missing-self" immunosurveillance by NK cells.

19 licensed G2(+) NK cells efficiently detected missing-self MHC cues on viral targets, which elicited c

20 nition strategies distinct from detection of missing self-MHC molecules by NK cells.

21 hibit NK cell activation is the basis of the missing self model of NK cell function.

22 C1/C1 combination expected to allow licensed missing self NK cell killing of index partners' cells.

23 geneic cell therapy, and the recognition of "missing-self" on target cells is crucial for promoting N

24 totoxicity against tumor cells representing "missing-self" or "induced-self." Lack of Bcl10 completel

25 ice have a recessive trait that perturbs the missing self reaction, as well as NKG2D-dependent respon

26 KLRG1 mediates missing self recognition by binding to a highly conserve

27 The impaired missing self recognition could not be overcome through c

28 Structural studies of missing self recognition have focused on NK receptors th

29 Missing self recognition of MHC class I molecules is med

30 Thus, DGKzeta knockout mice display improved missing self recognition, as evidenced by enhanced rejec

31 ng NKR-P1B(lo) NK subset and MHC-I-dependent missing-self recognition intact.

32 In contrast, MHC-I-dependent missing-self recognition is preserved in Nkrp1b(-/-) mic

33 a role for NKR-P1B(B6) in MHC-I-independent missing-self recognition of Clr-b in vivo.

34 ndant role for NKR-P1B:Clr-b interactions in missing-self recognition of normal hematopoietic cells a

35 tibility complex class I (MHC-I)-independent missing-self recognition system that monitors cellular C

36 B in NK cell tolerance and MHC-I-independent missing-self recognition.

37 ol of carcinogenesis through MHC-I-dependent missing-self recognition.

38 A- tumor cells during education for improved missing-self recognition.

39 es to the cell surface, presumably to avoid "missing self" recognition.

40 ells in the killing of allogeneic cells via "missing self" recognition.

41 ptors play a vital role in NK cell-mediated "missing-self" recognition, which contributes to NK cell

42 his receptor-ligand system in a new form of "missing self-recognition" of tumor cells.

43 rant NK cells optimally suited for efficient missing self-recognition.

44 th C57BL/6 mice, indicated that the impaired missing self rejection (IMSR) NK cell defect was a reces

45 Enhancement in missing-self response between NK subsets varied substant

46 the NK subsets displaying diverse levels of missing-self response, a system that reduces the presenc

47 n-regulated cell surface class I (i.e., the "missing self"-response).

48 Here we show that this 'missing-self' response can be prevented by forced expres

49 In contrast, missing-self responses were increased in the absence of

50 -associated antigens while permitting rapid "missing self"-responses to unsialylated multimeric antig

51 Cd226(-/-) mice have missing self-responses and NK cells with a normal recept

52 retenses" disrupts recognition of tumor cell missing self, thereby impairing cytotoxicity and IFN-gam

53 classically associated with the detection of missing self through loss of their respective MHC ligand