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1 nesis of autoimmunity and lymphomagenesis of autoimmune lymphoproliferative syndrome.
2 tients with systemic lupus erythematosus and autoimmune lymphoproliferative syndrome.
3 e classified the disease as a variant of the autoimmune lymphoproliferative syndrome.
4 disease to differentiate this disorder from autoimmune lymphoproliferative syndrome.
5 th Fas-induced lymphocyte apoptosis in human autoimmune lymphoproliferative syndrome.
6 ade FADD a candidate susceptibility gene for autoimmune lymphoproliferative syndrome.
7 ation and autoimmune cytopenias characterise autoimmune lymphoproliferative syndrome.
9 of mTOR activation in iMCD was comparable to autoimmune lymphoproliferative syndrome, a disease drive
12 Fas) receptor occur in most individuals with autoimmune lymphoproliferative syndrome (ALPS) and domin
14 ts in lymphocyte apoptosis that underlie the autoimmune lymphoproliferative syndrome (ALPS) are usual
17 tions of the Fas gene can result in a severe autoimmune lymphoproliferative syndrome (ALPS) in humans
37 , immunological, and clinical aspects of the autoimmune lymphoproliferative syndrome (ALPS) met in Be
38 ice et al document a 20-year experience with autoimmune lymphoproliferative syndrome (ALPS) patients
39 T cells with a phenotype similar to that in autoimmune lymphoproliferative syndrome (ALPS) patients.
42 ressing Fas mutations from patients with the autoimmune lymphoproliferative syndrome (ALPS) reveals t
45 al. explore somatic changes in patients with autoimmune lymphoproliferative syndrome (ALPS), a congen
46 ligand or caspase-10 underlie most cases of autoimmune lymphoproliferative syndrome (ALPS), a human
48 ototype for human apoptosis disorders is the autoimmune lymphoproliferative syndrome (ALPS), which is
54 oss-of-function FAS or FASLG mutations cause autoimmune-lymphoproliferative syndrome (ALPS) character
56 d exome sequencing in a patient with NDM and autoimmune lymphoproliferative syndrome and his unrelate
57 have revealed an ever-expanding spectrum of autoimmune lymphoproliferative syndrome and its major co
58 Gadd45gamma spontaneously developed signs of autoimmune lymphoproliferative syndrome and systemic lup
59 sociated with inherited human mutations: the autoimmune lymphoproliferative syndrome and the caspase-
60 mycobacterial diseases, Hyper-IgM syndrome, autoimmune lymphoproliferative syndrome, and GATA-2 defi
61 el homozygous mutation in ITK presented with autoimmune lymphoproliferative syndrome, and had impaire
62 with idiopathic CD4 lymphopenia, people with autoimmune lymphoproliferative syndrome, and healthy vol
65 n humans, fas mutations result in a familial autoimmune lymphoproliferative syndrome, but defects in
69 tosus, common variable immunodeficiency, and autoimmune lymphoproliferative syndromes, hemophagocytic
70 for caspase-10, previously implicated in the autoimmune lymphoproliferative syndrome, in death recept
72 haring these manifestations have been termed autoimmune lymphoproliferative syndrome-like diseases, a
73 ed-coil domain of STAT5B that presented with autoimmune lymphoproliferative syndrome-like features.
75 After biomarker and genetic assessments, autoimmune lymphoproliferative syndrome was diagnosed in
76 eceptor FAS(1,2) or its ligand FASL(3) cause autoimmune lymphoproliferative syndrome, whereas mutatio
77 d for patients with biomarkers indicative of autoimmune lymphoproliferative syndrome, while IEI panel
78 inically significant immunodeficiency and an autoimmune lymphoproliferative syndrome with marked pred
79 suggests potential treatments for lupus and autoimmune lymphoproliferative syndrome, without comprom