ライフサイエンスコーパス: MAIDS

1 lly, CD22 deficiency was found to accelerate MAIDS development.

2 Immune activation in murine AIDS (MAIDS) has been suggested to involve a superantigen (SAG

3 mmunodeficiency syndrome termed murine AIDS (MAIDS) in susceptible strains of mice, such as C57BL/6 (

4 Murine AIDS (MAIDS) induced by infection of C57BL/6 mice with a mixtu

5 defective virus responsible for murine AIDS (MAIDS) induces B-cell activation, proliferation, and dif

6 The immunodeficiency syndrome murine AIDS (MAIDS), caused by the BM5 retrovirus preparation, involv

7 This disease, murine AIDS (MAIDS), is inhibited by in vivo anti-CD154 monoclonal an

8 ficiency following infection of murine AIDS (MAIDS)-resistant mice with the LP-BM5 mixture of murine

9 ed immunodeficiency, designated murine AIDS (MAIDS).

10 mmunodeficiency syndrome called murine AIDS (MAIDS).

11 mmunodeficiency syndrome called murine AIDS (MAIDS).

12 , this syndrome has been called murine AIDS (MAIDS).

13 d lymphoproliferation, known as murine AIDS (MAIDS).

14 CD4 T cells, B6.nude mice develop full-blown MAIDS.

15 om CD154 knockout, B6 donors displayed clear MAIDS after LP-BM5 infection.

16 Because the decreased MAIDS pathogenesis could not be attributed to inhibition

17 6 expression: CD80/CD86(-/-) B6 mice develop MAIDS after LP-BM5 infection.

18 lls from wild-type B6 donors did not develop MAIDS after LP-BM5 infection.

19 Infected CR2(-/-) mice developed MAIDS with a time course and severity indistinguishable

20 phocytes were significantly decreased during MAIDS, by approximately 100-fold, from perforin mRNA lev

21 ed eyes destined to develop retinitis during MAIDS also showed a significant decrease in perforin mRN

22 that susceptibility to MCMV retinitis during MAIDS correlates with a decrease in the perforin cytotox

23 pyroptosis participate simultaneously during MAIDS-related MCMV retinitis, and all may play a role du

24 pecifically with regard to CD154 expression, MAIDS-insusceptible B6 nude mice reconstituted with high

25 requirement for CD154-CD40 interactions for MAIDS induction and progression can be accounted for by

26 upon LP-BM5 infection was not necessary for MAIDS.

27 ide the CD154 and CD40 expression needed for MAIDS induction.

28 CD4 T helper effector cells are required for MAIDS induction and progression of viral pathogenesis.

29 CD40 molecular interactions are required for MAIDS.

30 ssion of the defective virus responsible for MAIDS was enhanced in spleens of the knockouts in compar

31 Furthermore, MAIDS-resistant BALB/cByJ mice also generated secondary

32 e perforin mutation were diagnosed as having MAIDS by 5 to 8 weeks after infection by the criteria of

33 e with retrovirus-induced immunosuppression (MAIDS), we initially investigated MCMV-infected eyes for

34 yze the role of CD19, CD21, Vav, and CD22 in MAIDS, we infected mice deficient in CD19, CD21 (CR2), V

35 Anergy of CD4 T cells in MAIDS appears to be different from that seen in other sy

36 tes that once anergy has been established in MAIDS, it cannot be reversed by providing costimulation

37 est that this CD4 T cell immunodeficiency in MAIDS includes a TCR-induced program of activation-induc

38 e responsible for CD4 lymphoproliferation in MAIDS.

39 t express CD154 or CD40 for LP-BM5 to induce MAIDS.

40 also relatively resistant to LP-BM5-induced MAIDS, became susceptible to LP-BM5-induced disease afte

41 initiation and progression of LP-BM5-induced MAIDS.

42 onoclonal antibody (MAb) treatment inhibited MAIDS symptoms in LP-BM5-infected wild-type mice when ei

43 sponded quickly after adoptive transfer into MAIDS-infected hosts, becoming activated and proliferati

44 ion rendered genetically susceptible B6 mice MAIDS resistant.

45 d immunodeficiency syndrome in C57BL/6 mice (MAIDS) and impairs learning and memory without gross mot

46 MCMV-infected eyes of MAIDS-10 mice, but not MAIDS-4 mice, showed evidence of significant increases i

47 this possibility, we examined development of MAIDS in mice deficient in CD4 (CD4 knockout), in which

48 The development of MAIDS is associated with increased B-cell lymphoblast pr

49 IL-4 treatment to inhibit the development of MAIDS pathology.

50 The development of MAIDS requires CD4(+) T cells and MHC class II expressio

51 leukin-10 exhibited a delayed development of MAIDS-related pathology and maintained T-cell responsive

52 4 T cells are critical to the development of MAIDS.

53 and/gp39, are involved in the development of MAIDS.

54 and gp39 are critical to the development of MAIDS.

55 -associated molecules, MCMV-infected eyes of MAIDS-10 mice showed significant amounts of tumor necros

56 dies demonstrated that MCMV-infected eyes of MAIDS-10 mice, but not MAIDS-4 mice, showed evidence of

57 to retinal disease in MCMV-infected eyes of MAIDS-10 mice.

58 Whereas MCMV-infected eyes of MAIDS-4 mice showed little evidence of apoptosis-associa

59 ation and immunodeficiency, the hallmarks of MAIDS, developed with comparable kinetics and degree in

60 ion to substantially reduce the induction of MAIDS.

61 oped a short term adoptive transfer model of MAIDS to examine the requirements for the CD4 T cell res

62 revious reports have shown that the onset of MAIDS depends on the presence of both CD4+ T cells and B

63 ired for normal induction and progression of MAIDS.

64 d both for the initiation and progression of MAIDS.

65 ppressed the development of typical signs of MAIDS including splenomegaly, lymphadenopathy, and hyper

66 this syndrome has been named murine AIDS, or MAIDS.

67 tion of Th2-associated cytokines may promote MAIDS pathology, while Th1-associated cytokines may help

68 As a result, MAIDS-associated splenomegaly, hypergammaglobulinemia, g

69 Similarly, MAIDS did not develop in B6.nude mice.

70 tope(s) that is especially prevalent on such MAIDS tumor cells, indicating the potential to mount a p

71 Th1 and Th2 CD4 T cells equally supported MAIDS induction.

72 etrovirus-induced immunodeficiency syndrome (MAIDS) exhibited a frequency and severity of MCMV retini

73 Murine acquired immunodeficiency syndrome (MAIDS) is a fatal disease induced by a mixture of retrov

74 d murine acquired immunodeficiency syndrome (MAIDS), characterized by lymphoproliferation and immunod

75 etrovirus-induced immunodeficiency syndrome, MAIDS.

76 of large numbers of CD4 T cells suggest that MAIDS involves a disruption of the balance of homeostati

77 tion of B and CD4 T cells that is central to MAIDS pathogenesis requires ligation of CD154 on CD4 T c

78 dent functions of CD8+ T cells contribute to MAIDS resistance but that other, non-CD8-dependent mecha

79 ther evaluate the mechanisms contributing to MAIDS resistance, we studied mice lacking CD8+ T cells o

80 different strain combinations, resistance to MAIDS was contingent on the presence in individual anima

81 In contrast to wild-type, MAIDS-resistant controls, B10.A mice homozygous for the

82 Mtv- mice developed typical MAIDS, excluding a requirement for Mtv-encoded SAGs in t

83 h MAIDS of 4 weeks' (MAIDS-4) and 10 weeks' (MAIDS-10) duration, which were resistant and susceptible

84 ed molecules in mice with MAIDS of 4 weeks' (MAIDS-4) and 10 weeks' (MAIDS-10) duration, which were r

85 ed with whole eyes of untreated animals with MAIDS (4.5 log10).

86 , none (0%) of PEG-IL-2-treated animals with MAIDS showed classic MCMV retinitis.

87 in whole eyes of PEG-IL-2-treated mice with MAIDS (2.8 log10), but not in whole eyes of IL-12-treate

88 We conclude that B cells from mice with MAIDS activate unique IL-4- and STAT6-independent signal

89 the cognitive deficits observed in mice with MAIDS and other retrovirus-induced encephalopathies.

90 Moreover, mice with MAIDS exhibited an abnormal histological distribution of

91 plus PMA, anergic CD4 T cells from mice with MAIDS fail to progress through the cell cycle (G0/G1 arr

92 this hypothesis, CD4 T cells from mice with MAIDS failed to regulate the homeostatic division of nai

93 apoptosis-associated molecules in mice with MAIDS of 4 weeks' (MAIDS-4) and 10 weeks' (MAIDS-10) dur

94 Adult C57BL/6 mice with MAIDS of 8 weeks' duration were treated with either a si

95 urine recombinant IL-12; untreated mice with MAIDS received phosphate-buffered saline.

96 80% of IL-12-treated and untreated mice with MAIDS showed histopathologic features consistent with cl

97 did not respond in H-2M-deficient mice with MAIDS, suggesting that disease requires recognition of s

98 L-2 and IL-12 on MCMV-retinitis in mice with MAIDS, the authors conclude that cytokine immunotherapy

99 -inoculated eyes of normal mice or mice with MAIDS.

100 alent in normal and IL-4-deficient mice with MAIDS.

101 ve to glutamatergic stimulation in mice with MAIDS.