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 a molecule commonly lost on stressed cells ("missing-self").

3 o induces NK cell reactivity or tolerance to missing-self.

4 d rejection of MHC-I-deficient cells through missing-self.

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

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

7 nor and recipient can create a situation of "missing self" allowing NK cells to kill graft ECs.

8 study investigated whether the condition of missing self amplifies DSA-dependent NK cell activation

9 We explored associations of missing self and gene polymorphisms determining the phen

10 Missing self and lesions of cellular rejection were not

11 cus is on natural killer cell activation via missing self and monocyte activation through the signal

12 Missing self and NK-cell genetics may contribute to MVI,

13 cells demonstrated dampened ADCC in both the missing-self and KIR-ligand matched settings, even in th

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

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

16 Missing self associated with transplant glomerulopathy a

17 The assessment of missing self at the time of diagnosis of chronic AMR ide

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

19 ility of cDC2 to be activated by circulating missing self-CD47 cells and to integrate multiple red bl

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

21 consistently showed more potent ADCC in the missing-self context despite lower levels of CD16 expres

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

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

24 nded to be more frequent among patients with missing self >=2 (hazard ratio 1.97; 95% CI, 0.89-4.37;

25 nuria (HR: 7.24; P=0.01) and the presence of missing self (HR: 3.57; P=0.04) were independent predict

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

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

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

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

30 er, are not autoreactive as predicted by the missing-self hypothesis.

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

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

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

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

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

36 Systematic evaluation of missing self improves understanding of HLA-DSA-negative

37 We identified missing self in 399 of 924 transplantations.

38 s sufficient to license NK cells and mediate missing-self in vivo.

39 A consensus definition of genetic missing self is proposed, necessitating both donor and r

40 IV-infected cells activated NK cells through missing-self mechanisms due to the downmodulation of cel

41 cell-specific activating ligand, m157, with missing self MHC-I resulted in complete graft rejection,

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

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

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

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

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

47 the absence of self HLA class I molecules ("missing self") on allograft endothelial cells.

48 s of ADCC than uneducated NK cells in either missing-self or KIR-ligand matched settings at saturatin

49 Conversely, missing self (OR 1.40; 95% CI, 1.08-1.80; P = 0.011) and

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

51 activation is mediating the process through "missing-self" or other activating mechanisms.

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

53 setting, inflammation triggered substantial missing-self reactivity.

54 and tolerance to missing-self without overt missing-self reactivity.

55 ll fraction of hematopoietic cells triggered missing-self reactivity.

56 lling in vivo and that inflammation promotes missing-self reactivity.

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

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

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

60 Missing self recognition of MHC class I molecules is med

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

62 ted cell susceptible to NK cell killing upon missing self recognition.

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

64 Missing-self recognition involves NK cell sensing of the

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

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

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

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

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

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

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

72 ic Ag receptor T cells by overcoming NK cell missing-self recognition.

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

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

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

76 t down-regulate MHC class I (MHC-I) through "missing-self" recognition.

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

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

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

80 ismatched CD8(+) T cells without triggering 'missing-self' rejection by natural killer cells.

81 in the presence of population structure and missing self-reported race and ethnicities in diverse WG

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

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

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

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

86 gh the absence of B2M is expected to trigger missing-self responses by host natural killer (NK) cells

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

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

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

90 However, missing self's clinical importance as a nonhumoral trigg

91 Missing self specifically and cumulatively increases MVI

92 y49A alone on an H-2D(d) background restored missing-self target cell rejection, NK cell licensing, a

93 xpression of all Ly49s were unable to reject missing-self target cells in vivo, were defective in NK

94 ls with heightened effector function against missing self-targets is not known.

95 Missing self, the inability of donor endothelial cells t

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

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

98 endothelial cells confirmed that addition of missing self to DSA-induced NK cell activation increased

99 Co-occurrence of missing self types had an additive effect in increasing

100 nts with MVI; 28 of the 146 had at least two missing self types.

101 Missing self was defined as the absence of A3/A11, Bw4,

102 ndent chronic AMR (n=62, 46%), those in whom missing self was identified through donor and recipient

103 NK cell hyporesponsiveness and tolerance to missing-self without overt missing-self reactivity.

104 ) T cells predominately induced tolerance to missing-self without resetting NK cell responsiveness.