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1 responses are impaired in most patients with common variable immunodeficiency.
2 ession is similarly decreased in humans with common variable immunodeficiency.
3 ere, primary immunodeficiency reminiscent of common variable immunodeficiency.
4 ment similar to those found in patients with common variable immunodeficiency.
5 phoproliferative disease and severe cases of common variable immunodeficiency.
6 efects in patients previously diagnosed with common variable immunodeficiency.
7 ar antibodies, sinopulmonary infections, and common variable immunodeficiency.
8 ve been found to be mutated in patients with common variable immunodeficiency.
9 rom a poliomyelitis patient from Taiwan with common variable immunodeficiency.
10 est risk was associated with T-cell PIDs and common variable immunodeficiency.
11 fferentiation in familial IgA deficiency and common variable immunodeficiency.
12 tions in LRBA Biallelic LRBA mutations cause common variable immunodeficiency-8; however, NDM has not
13 was highly similar to that of patients with common variable immunodeficiency and a defect in B-cell
14 ilin ligand interactor (TACI), contribute to common variable immunodeficiency and autoimmunity in hum
15 on, shown through the study of patients with common variable immunodeficiency and hyper IgM syndrome,
16 ustrate the heterogeneous molecular basis of common variable immunodeficiency and indicate the value
17 is review discusses the latest insights into common variable immunodeficiency and uses common variabl
18 everal primary immunodeficiencies, including common variable immunodeficiency and Wiskott-Aldrich syn
20 and additional family members suffering from common variable immunodeficiency and/or selective IgA de
21 n a clinical picture that is consistent with common variable immunodeficiency, and as many as 10% of
22 orders such as systemic lupus erythematosus, common variable immunodeficiency, and autoimmune lymphop
23 to common variable immunodeficiency and uses common variable immunodeficiency as a model to examine t
25 ound that 4 of 19 unrelated individuals with common variable immunodeficiency (CVID) and 1 of 16 indi
30 ma cells, and almost 10% of individuals with common variable immunodeficiency (CVID) express either t
47 in patients with autoimmune diseases and in common variable immunodeficiency (CVID) patients who are
50 the HVR of control patients to patients with common variable immunodeficiency (CVID) where the effect
52 arisons between patients with GS, those with common variable immunodeficiency (CVID), and those with
54 ts with multilineage cytopenias secondary to common variable immunodeficiency (CVID), Evans syndrome
55 al profile of CD4 T cells from patients with common variable immunodeficiency (CVID), including produ
65 le nucleotide polymorphisms in patients with common variable immunodeficiency disorder (CVID), which
66 mplex polygenic disorders, most commonly the common variable immunodeficiency disorders (CVIDs), pred
69 ysis of the proportion of any combination of common variable immunodeficiency, IgG deficiency, IgA de
70 -telangiectasia, Nijmegen-breakage-syndrome, common variable immunodeficiency, immunoglobulin A defic
74 s human PRKCD deficiency as a novel cause of common variable immunodeficiency-like B-cell deficiency
75 e defects affect a minority of patients with common variable immunodeficiency only, future genetic re
76 tterns in gut biopsies from individuals with common variable immunodeficiency or with HIV infection a
78 children <2 y, the asplenic, and a subset of common variable immunodeficiency patients, are profoundl
79 rated IRF4 to be deregulated in B cells from common variable immunodeficiency patients, contributing
82 tic assessment in paediatric patients with a common variable immunodeficiency phenotype, to establish
84 Newly identified disease genes within the common variable immunodeficiency population, have advanc
86 present the different clinical phenotypes of common variable immunodeficiency, review recent genetic
87 ith unusually frequent bacterial infections, common variable immunodeficiency should always be consid
88 day period from a poliomyelitis patient with common variable immunodeficiency syndrome (a defect in a
89 t poliovirus infection in an individual with common variable immunodeficiency, using oral immunoglobu
90 ional features not typically associated with common variable immunodeficiency were diagnosed only lat
92 nted with a phenotype resembling early-onset common variable immunodeficiency, while extra-immunologi
95 the diagnosis and treatment of patients with common variable immunodeficiency, with suggestions for t
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