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1 asplenia, and 2 of Bruton disease (X-linked agammaglobulinemia).
2 and represent an autosomal dominant form of agammaglobulinemia.
3 ions in BTK cause a severe B-cell defect and agammaglobulinemia.
4 mal in BTK, the gene that underlies X-linked agammaglobulinemia.
5 ion might play a role in X chromosome-linked agammaglobulinemia.
6 aling culminate in X-linked and non-X-linked agammaglobulinemia.
7 y immunodeficiency diseases characterized by agammaglobulinemia.
8 in human B-cell ontogeny leading to X-linked agammaglobulinemia.
9 that mutations in Igalpha can be a cause of agammaglobulinemia.
10 results in a clinical phenotype of X-linked agammaglobulinemia.
11 the human btk gene are the cause of X-linked agammaglobulinemia, a male immune deficiency disorder ch
12 s in a variety of genes can cause congenital agammaglobulinemia and a failure of B cell development.
13 terminal LRRs was reported in a patient with agammaglobulinemia and absent B cells and was demonstrat
14 Approximately 90% of patients with isolated agammaglobulinemia and failure of B cell development hav
20 tyrosine kinase (Btk) causes human X-linked agammaglobulinemia and murine X-linked immunodeficiency
21 he novel entity of SCID was characterized by agammaglobulinemia and profoundly deficient T-cell funct
22 logical conditions such as myeloma, X-linked agammaglobulinemia, and HIV infection may provide insigh
23 The patients had hypogammaglobulinemia or agammaglobulinemia, and their peripheral-blood B cells a
24 ommon variable immunodeficiency and X-linked agammaglobulinemia, bacterial organisms are the most com
25 hoproliferative disease (XLP) is progressive agammaglobulinemia, caused by the absence of a functiona
26 mice recapitulate a central feature of human agammaglobulinemia: CVB establishes chronic infection in
27 the case of a 34-year-old man with X-linked agammaglobulinemia from Australia suffering from 3 years
28 ich is mutated in the human disease X-linked agammaglobulinemia, has been shown to interact with PI(3
29 ts in the immunodeficiency diseases X-linked agammaglobulinemia in humans and X-linked immunodeficien
33 ted by the primary immune disorder, X-linked agammaglobulinemia in which patients are prone to chroni
34 se (Btk) result in a disease called X-linked agammaglobulinemia, in which there is a profound decreas
37 tyrosine kinase (Btk) is mutated in X-linked agammaglobulinemia patients and plays an essential role
39 y the X-linked immunodeficiency and X-linked agammaglobulinemia phenotypes of mice and men that expre
41 T cell deficiencies, but not with congenital agammaglobulinemia, suggesting the importance of T cell
43 ment of gene therapy strategies for X-linked agammaglobulinemia, the immunodeficiency associated with
44 nfrequent, and acquired resistance to Bruton agammaglobulinemia tyrosine kinase (BTK) inhibition is b
45 b resistance to acquired mutations in Bruton agammaglobulinemia tyrosine kinase (BTK), the target of
46 ation was reported in patients with X-linked agammaglobulinemia, underscoring the important role of B
47 se (BTK) mutations as the cause for X-linked agammaglobulinemia was a milestone in understanding the
48 patient previously thought to have X-linked agammaglobulinemia was found to have an amino acid subst
50 of the Btk PH domain, which causes X-linked agammaglobulinemia, was introduced into the fluorescent
51 n individuals with the diagnosis of X-linked agammaglobulinemia were analyzed for mutations in Bruton
52 h chronic meningoencephalitis and underlying agammaglobulinemia were examined to determine enterovira
53 n the bone marrow present early in life with agammaglobulinemia, whereas incomplete antibody deficien
54 a and absent B cells are males with X-linked agammaglobulinemia, which is caused by mutations in the
55 l of N addition appears aberrant in X-linked agammaglobulinemia, which may exacerbate the block in B
56 elopment and patients with presumed X-linked agammaglobulinemia who did not have mutations in Btk.
57 ed immune deficiency, X-linked and autosomal agammaglobulinemia, Wiskott-Aldrich syndrome, and other
58 port spontaneous emergence of non-sex-linked agammaglobulinemia with B-cell deficiency and cutaneous
60 ombined immunodeficiency (SCID) and X-linked agammaglobulinemia (XLA) are inborn errors of immune fun
64 's tyrosine kinase (btk) gene cause X-linked agammaglobulinemia (XLA) in humans and X-linked immune d
65 utations in Btk are responsible for X-linked agammaglobulinemia (XLA) in humans and X-linked immunode
66 uton's tyrosine kinase (Btk) causes X-linked agammaglobulinemia (XLA) in humans and X-linked immunode
67 n's tyrosine kinase (Btk) result in X-linked agammaglobulinemia (XLA) in humans and X-linked immunode
68 ause the B cell deficiency diseases X-linked agammaglobulinemia (XLA) in humans and X-linked immunode
69 lt in the B cell immunodeficiencies X-linked agammaglobulinemia (XLA) in humans and X-linked immunode
70 lt in the B cell immunodeficiencies X-linked agammaglobulinemia (XLA) in humans and X-linked immunode
77 id lines derived from patients with X-linked agammaglobulinemia (XLA) lacking Btk expression, as well
78 d cultured cells from patients with X-linked agammaglobulinemia (XLA) suggested defective TLR-driven
79 In 1993, two groups showed that X-linked agammaglobulinemia (XLA) was due to mutations in a tyros
80 ith wortmannin and in patients with X-linked agammaglobulinemia (XLA), a condition caused by a lack o
88 mbined immune deficiency (SCID) and X-linked agammaglobulinemia (XLA); however, gain-of-function muta
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