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1 tients with systemic lupus erythematosus and autoimmune lymphoproliferative syndrome.
2 e classified the disease as a variant of the autoimmune lymphoproliferative syndrome.
3 disease to differentiate this disorder from autoimmune lymphoproliferative syndrome.
4 nesis of autoimmunity and lymphomagenesis of 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.
9 Fas) receptor occur in most individuals with autoimmune lymphoproliferative syndrome (ALPS) and domin
11 ts in lymphocyte apoptosis that underlie the autoimmune lymphoproliferative syndrome (ALPS) are usual
13 tions of the Fas gene can result in a severe autoimmune lymphoproliferative syndrome (ALPS) in humans
30 , immunological, and clinical aspects of the autoimmune lymphoproliferative syndrome (ALPS) met in Be
31 ice et al document a 20-year experience with autoimmune lymphoproliferative syndrome (ALPS) patients
32 T cells with a phenotype similar to that in autoimmune lymphoproliferative syndrome (ALPS) patients.
35 ressing Fas mutations from patients with the autoimmune lymphoproliferative syndrome (ALPS) reveals t
38 al. explore somatic changes in patients with autoimmune lymphoproliferative syndrome (ALPS), a congen
39 ligand or caspase-10 underlie most cases of autoimmune lymphoproliferative syndrome (ALPS), a human
41 ototype for human apoptosis disorders is the autoimmune lymphoproliferative syndrome (ALPS), which is
47 d exome sequencing in a patient with NDM and autoimmune lymphoproliferative syndrome and his unrelate
48 have revealed an ever-expanding spectrum of autoimmune lymphoproliferative syndrome and its major co
49 Gadd45gamma spontaneously developed signs of autoimmune lymphoproliferative syndrome and systemic lup
50 sociated with inherited human mutations: the autoimmune lymphoproliferative syndrome and the caspase-
52 n humans, fas mutations result in a familial autoimmune lymphoproliferative syndrome, but defects in
55 tosus, common variable immunodeficiency, and autoimmune lymphoproliferative syndromes, hemophagocytic
56 for caspase-10, previously implicated in the autoimmune lymphoproliferative syndrome, in death recept
58 ed-coil domain of STAT5B that presented with autoimmune lymphoproliferative syndrome-like features.
59 suggests potential treatments for lupus and autoimmune lymphoproliferative syndrome, without comprom
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