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2 cell activation, and convey to patients with common variable immune deficiency (CVID) an increased ri
6 ICOSL, or SH2D1, and are best classified as common variable immune deficiency (CVID), although other
9 mortality statistics from 473 subjects with common variable immune deficiency followed over 4 decade
11 cy has been reported as a monogenic cause of common variable immune deficiency with features of immun
12 tivator and CAML interactor (TACI) result in common variable immune deficiency, a syndrome marked by
13 mechanism explaining the primary features of common variable immune deficiency, exquisite vulnerabili
14 ther disorders, including Evans syndrome and common variable immune deficiency, have been found to ha
15 ed immunodeficiency syndrome (AIDS); one had common variable immune deficiency; and 18 were receiving
16 ound that 4 of 19 unrelated individuals with common variable immunodeficiency (CVID) and 1 of 16 indi
21 ma cells, and almost 10% of individuals with common variable immunodeficiency (CVID) express either t
38 in patients with autoimmune diseases and in common variable immunodeficiency (CVID) patients who are
41 the HVR of control patients to patients with common variable immunodeficiency (CVID) where the effect
43 arisons between patients with GS, those with common variable immunodeficiency (CVID), and those with
45 ts with multilineage cytopenias secondary to common variable immunodeficiency (CVID), Evans syndrome
46 al profile of CD4 T cells from patients with common variable immunodeficiency (CVID), including produ
54 was highly similar to that of patients with common variable immunodeficiency and a defect in B-cell
55 ilin ligand interactor (TACI), contribute to common variable immunodeficiency and autoimmunity in hum
56 on, shown through the study of patients with common variable immunodeficiency and hyper IgM syndrome,
57 ustrate the heterogeneous molecular basis of common variable immunodeficiency and indicate the value
58 is review discusses the latest insights into common variable immunodeficiency and uses common variabl
59 everal primary immunodeficiencies, including common variable immunodeficiency and Wiskott-Aldrich syn
61 and additional family members suffering from common variable immunodeficiency and/or selective IgA de
62 to common variable immunodeficiency and uses common variable immunodeficiency as a model to examine t
66 le nucleotide polymorphisms in patients with common variable immunodeficiency disorder (CVID), which
67 mplex polygenic disorders, most commonly the common variable immunodeficiency disorders (CVIDs), pred
73 e defects affect a minority of patients with common variable immunodeficiency only, future genetic re
74 tterns in gut biopsies from individuals with common variable immunodeficiency or with HIV infection a
76 children <2 y, the asplenic, and a subset of common variable immunodeficiency patients, are profoundl
77 rated IRF4 to be deregulated in B cells from common variable immunodeficiency patients, contributing
80 tic assessment in paediatric patients with a common variable immunodeficiency phenotype, to establish
82 Newly identified disease genes within the common variable immunodeficiency population, have advanc
84 ith unusually frequent bacterial infections, common variable immunodeficiency should always be consid
85 day period from a poliomyelitis patient with common variable immunodeficiency syndrome (a defect in a
86 ional features not typically associated with common variable immunodeficiency were diagnosed only lat
90 n a clinical picture that is consistent with common variable immunodeficiency, and as many as 10% of
91 orders such as systemic lupus erythematosus, common variable immunodeficiency, and autoimmune lymphop
92 ysis of the proportion of any combination of common variable immunodeficiency, IgG deficiency, IgA de
93 -telangiectasia, Nijmegen-breakage-syndrome, common variable immunodeficiency, immunoglobulin A defic
94 present the different clinical phenotypes of common variable immunodeficiency, review recent genetic
95 t poliovirus infection in an individual with common variable immunodeficiency, using oral immunoglobu
96 nted with a phenotype resembling early-onset common variable immunodeficiency, while extra-immunologi
97 the diagnosis and treatment of patients with common variable immunodeficiency, with suggestions for t
98 tions in LRBA Biallelic LRBA mutations cause common variable immunodeficiency-8; however, NDM has not
99 s human PRKCD deficiency as a novel cause of common variable immunodeficiency-like B-cell deficiency
111 observation of large differences due to less common variables indicates the complex nature of the for
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