ライフサイエンスコーパス: hypergammaglobulinemia

1 rentiation, compromised B cell function, and hypergammaglobulinemia.

2 with frequent germinal center reactions and hypergammaglobulinemia.

3 d with B cell activation and exhaustion, and hypergammaglobulinemia.

4 ice with AdTACI prevented the development of hypergammaglobulinemia.

5 including splenomegaly, lymphadenopathy, and hypergammaglobulinemia.

6 burden, cachexia, massive splenomegaly, and hypergammaglobulinemia.

7 ph nodes; hepatosplenomegaly; and polyclonal hypergammaglobulinemia.

8 hadenopathy, hepatomegaly, splenomegaly, and hypergammaglobulinemia.

9 ntibody-secreting cell (ASC) frequencies and hypergammaglobulinemia.

10 ggerated in aging mice that normally develop hypergammaglobulinemia.

11 All had hypergammaglobulinemia (3.0 +/- 1.0 g/dL) and autoantibo

12 with remodeling of lymphoid architecture and hypergammaglobulinemia, although the mechanisms leading

13 on chromosome 1 (peak at 106 cM), linked to hypergammaglobulinemia; an NZB locus on chromosome 5 (Nb

14 These AND alpha beta T cells induced hypergammaglobulinemia and autoantibody production, as s

15 T cell-intact mice, consisting of augmented hypergammaglobulinemia and autoantibody production, more

16 roles in the development of lupus-associated hypergammaglobulinemia and autoantibody production; howe

17 be an important factor in driving polyclonal hypergammaglobulinemia and elevated autoantibody titers

18 linked (or showed a trend for linkage) with hypergammaglobulinemia and IgG1, IgG2a, and/or IgG3 leve

19 h novel heterozygous CD95 mutations revealed hypergammaglobulinemia and immune-mediated cytopenias in

20 h known hallmarks of HIV-1 infection, namely hypergammaglobulinemia and increased frequencies of peri

21 osomal P autoantibodies and normalization of hypergammaglobulinemia and low C3/C4 levels.

22 evelopment of lupus nephritis by suppressing hypergammaglobulinemia and renal disease.

23 rther, these autoreactive CD4+ T cells cause hypergammaglobulinemia and the production of autoantibod

24 vivo T cell cycling and activation, moderate hypergammaglobulinemia and, at low penetrance, anti-chro

25 minates in lymphadenopathy and splenomegaly, hypergammaglobulinemia, and autoantibodies.

26 or/memory T cells and IgG+ B cells, profound hypergammaglobulinemia, and autoantibody production.

27 f B cells resulting in lymphoid hyperplasia, hypergammaglobulinemia, and autoimmunity in neonatal pig

28 ells in peripheral lymphoid organs, moderate hypergammaglobulinemia, and deposited complexes in the k

29 low, progressive systemic immune activation, hypergammaglobulinemia, and enhanced germinal center for

30 ng immune complexes, immune complex disease, hypergammaglobulinemia, and high levels of antiviral ant

31 stations, including autoantibody production, hypergammaglobulinemia, and immune-complex renal disease

32 /-) mice developed more severe splenomegaly, hypergammaglobulinemia, and immunodeficiency than infect

33 mice develop splenomegaly, lymphadenopathy, hypergammaglobulinemia, and immunodeficiency; thus, this

34 ressive destruction of infected CD4 T cells, hypergammaglobulinemia, and loss of memory B cells.

35 gic sequelae, including lymphoproliferation, hypergammaglobulinemia, and overt systemic autoimmunity.

36 ng splenomegaly, multifocal lymphadenopathy, hypergammaglobulinemia, and plasmacytosis.

37 stream induction of germinal center B cells, hypergammaglobulinemia, and production of antilipid anti

38 hepatitis (based on histologic examination), hypergammaglobulinemia, and production of autoantibodies

39 terized by low sensitivity to bacterial LPS, hypergammaglobulinemia, and reduced secretion of proinfl

40 nuclear cell infiltration, hepatic fibrosis, hypergammaglobulinemia, anti-nuclear and anti-smooth mus

41 se that included leukocytosis, splenomegaly, hypergammaglobulinemia, antinuclear autoantibody and pro

42 Terminal differentiation of B cells and hypergammaglobulinemia are hallmarks of B-cell hyperacti

43 fested by the presence of autoantibodies and hypergammaglobulinemia, as well as clinical/serological

44 n to induce polyclonal B cell activation and hypergammaglobulinemia, as well as increased production

45 but they develop over time plasmacytosis and hypergammaglobulinemia, as well as systemic inflammation

46 mpaired and which may be responsible for the hypergammaglobulinemia associated with HIV disease.

47 uman systemic lupus erythematosus, including hypergammaglobulinemia, autoantibodies against DNA and s

48 model of lupus, including the development of hypergammaglobulinemia, autoantibodies including anti-do

49 sus-like autoimmune disease characterized by hypergammaglobulinemia, autoantibodies, lymphadenopathy,

50 oimmune disease indicator analyzed including hypergammaglobulinemia; autoantibodies including anti-DN

51 habeta T cells in conjunction with unaltered hypergammaglobulinemia, autoantibody production, and imm

52 ted autoimmunity, characterized by increased hypergammaglobulinemia, autoantibody production, and imm

53 All disease parameters, including hypergammaglobulinemia, autoantibody production, glomeru

54 MRL/lpr) mice consists of severe pan-isotype hypergammaglobulinemia, autoantibody production, lymphad

55 SLE in IL-21R-competent Yaa mice, including hypergammaglobulinemia, autoantibody production, reduced

56 to massive splenomegaly and lymphadenopathy, hypergammaglobulinemia, autoimmunity, B-cell lymphocytos

57 Hypergammaglobulinemia, but not PM, was associated with

58 lele of Roquin develop tumors accompanied by hypergammaglobulinemia by 6 months of age.

59 The generalized hypergammaglobulinemia characteristic of MRL-Fas(lpr) mi

60 Protein electrophoresis revealed hypergammaglobulinemia consistent with chronic inflammat

61 The transgenic mice also had hypergammaglobulinemia contributed by elevations of seru

62 which manifest excitotoxic brain lesions and hypergammaglobulinemia, for the presence of AMPA-recepto

63 on, accumulation of double-negative T cells, hypergammaglobulinemia G and A, and autoimmune cytopenia

64 As a result, MAIDS-associated splenomegaly, hypergammaglobulinemia, germinal center formation, and t

65 auses a persistent infection associated with hypergammaglobulinemia, high levels of antiviral antibod

66 syndrome, characterized by isotype-specific hypergammaglobulinemia, incompletely penetrant autoantib

67 piglets (PIPs), explaining why PRRSV-induced hypergammaglobulinemia is seen in all major isotypes.

68 racterized by splenomegaly, lymphadenopathy, hypergammaglobulinemia, loss of T and B cell function, a

69 nase-elevating virus of mice, develop severe hypergammaglobulinemia, lymph node adenopathy, and autoi

70 ne retroviruses cause profound splenomegaly, hypergammaglobulinemia, lymphadenopathy, and an immunode

71 ansplacental transfer of IgG3, adjusting for hypergammaglobulinemia, maternal malaria, and infant mal

72 ons, but placental malaria (PM) and maternal hypergammaglobulinemia might interfere with transplacent

73 Some B cell abnormalities include hypergammaglobulinemia, nonspecific B cell activation, c

74 to numerous B cell abnormalities, including hypergammaglobulinemia, nonspecific B cell activation, n

75 PM and hypergammaglobulinemia occurred in 60% and 54% of Alexis

76 and chronically infected people, whereas the hypergammaglobulinemia often present during chronic infe

77 cell phenotypic changes, hyperproliferation, hypergammaglobulinemia, or splenomegaly.

78 f a significant increase in splenic IL-4 and hypergammaglobulinemia primarily of the IgG1 isotype, wi

79 Immune defects in these mice include hypergammaglobulinemia, production of multiple autoantib

80 roviral isolate LP-BM5 induces splenomegaly, hypergammaglobulinemia, profound B- and T-cell immunodef

81 r Abs and IgG anti-chromatin autoantibodies, hypergammaglobulinemia, renal Ig deposition, and protein

82 l as extensive B cell hyperproliferation and hypergammaglobulinemia, resulting in splenomegaly and ly

83 We believe that the hypergammaglobulinemia results from the products of thes

84 Autoimmune features such as hypergammaglobulinemia, rheumatoid factor, and circulati

85 neous infections, plasma cell proliferation, hypergammaglobulinemia, severe deficiencies of leukocyte

86 Moreover, the pattern of hypergammaglobulinemia suggests that the requirement for

87 elop profound splenomegaly, lymphadenopathy, hypergammaglobulinemia, terminal B-cell lymphomas, and a

88 netic background, TSAd deficiency results in hypergammaglobulinemia that affects all immunoglobulin (

89 Hypergammaglobulinemia was associated with severe immune

90 Hypergammaglobulinemia was maintained with a switch from

91 ralized Ag-independent B cell activation and hypergammaglobulinemia with biased expansion of a subpop

92 ally deficient in CD152 (CTLA-4), polyclonal hypergammaglobulinemia with increased levels of systemic