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1 escribed by examining patients with familial hemophagocytic lymphohistiocytosis.
2 g them are Langerhans cell histiocytosis and hemophagocytic lymphohistiocytosis.
3 y results in several human diseases, such as hemophagocytic lymphohistiocytosis.
4 des, T-cell lymphoproliferative disease, and hemophagocytic lymphohistiocytosis.
5 mutations in Munc13-4 as a cause of familial hemophagocytic lymphohistiocytosis.
6 with familial and virus-associated reactive hemophagocytic lymphohistiocytosis.
7 are associated with some cases of CAEBV with hemophagocytic lymphohistiocytosis.
8 ked lymphoproliferative disease and familial hemophagocytic lymphohistiocytosis.
9 erest in discussing a specific treatment for hemophagocytic lymphohistiocytosis.
10 rimary immunodeficiencies including familial hemophagocytic lymphohistiocytosis.
11 ells, resulting in the development of lethal hemophagocytic lymphohistiocytosis.
12 o those implicated in the setting of primary hemophagocytic lymphohistiocytosis.
13 ppropriately classified as X-linked familial hemophagocytic lymphohistiocytosis.
14 equired to induce disease in mouse models of hemophagocytic lymphohistiocytosis.
15 tify Munc13-4, a protein mutated in familial hemophagocytic lymphohistiocytosis 3, as a WPB-tethering
16 mutations account for 20% to 40% of familial hemophagocytic lymphohistiocytosis, a fatal disease of e
17 ng mutations in these genes develop familial hemophagocytic lymphohistiocytosis, a primary immunodefi
18 chosocial outcomes in childhood survivors of hemophagocytic lymphohistiocytosis after hematopoietic s
19 nts with a clinically suspected diagnosis of hemophagocytic lymphohistiocytosis and found 28 patients
21 Although it has been proposed that in both hemophagocytic lymphohistiocytosis and macrophage activa
22 as well as (4) Rosai-Dorfman disease and (5) hemophagocytic lymphohistiocytosis and macrophage activa
23 ic benefits in preclinical disease models of hemophagocytic lymphohistiocytosis and multiple sclerosi
24 -eating macrophages, is seen in the disorder hemophagocytic lymphohistiocytosis and other inflammator
25 yperinflammatory syndromes, however, such as hemophagocytic lymphohistiocytosis and the newly classif
26 iated hydroa vacciniforme-like lymphoma with hemophagocytic lymphohistiocytosis, and 2 had EBV-positi
27 were to identify the frequency of secondary hemophagocytic lymphohistiocytosis, and the main prognos
29 ogic abnormalities in patients with familial hemophagocytic lymphohistiocytosis are decreased natural
30 e for treating some cases of type 2 familial hemophagocytic lymphohistiocytosis, based on the pharmac
31 atients admitted with suspected or diagnosed hemophagocytic lymphohistiocytosis, between January 1, 2
32 haracterized by immunodeficiency and a fatal hemophagocytic lymphohistiocytosis caused by impaired fu
33 D, STX11, or STXBP2 associated with familial hemophagocytic lymphohistiocytosis, CTL and NK cell degr
44 f PBMCs obtained from patients with familial hemophagocytic lymphohistiocytosis (FHL) to screen for b
45 Cytokine storm syndromes, such as familial hemophagocytic lymphohistiocytosis (FHL), are lethal dis
46 of patients, referred to as having familial hemophagocytic lymphohistiocytosis (FHL), have various u
49 -4, in which mutations cause type 3 familial hemophagocytic lymphohistiocytosis (FHL3), a fatal disea
50 (NK) cytotoxicity, and give rise to familial hemophagocytic lymphohistiocytosis (FHL4 or FHL5, respec
51 ive disorders collectively known as familial hemophagocytic lymphohistiocytosis (FHLH), all associate
52 about half of patients with severe forms of hemophagocytic lymphohistiocytosis have been developed.
53 cells and developed all clinical symptoms of hemophagocytic lymphohistiocytosis (HLH) after infection
54 ive T-cell activation and the fatal disorder hemophagocytic lymphohistiocytosis (HLH) after infection
55 ed to be associated with a high incidence of hemophagocytic lymphohistiocytosis (HLH) and a lack of l
56 he hyperinflammatory state characteristic of hemophagocytic lymphohistiocytosis (HLH) and macrophage
59 poietic stem cell transplantation (HSCT) for hemophagocytic lymphohistiocytosis (HLH) at the cost of
80 imary, genetic forms from secondary forms of hemophagocytic lymphohistiocytosis (HLH) is crucial for
82 iable clinical consequences, including fatal hemophagocytic lymphohistiocytosis (HLH) triggered predo
83 ns can improve the outcomes of patients with hemophagocytic lymphohistiocytosis (HLH) undergoing allo
84 thologically, MAS bears strong similarity to hemophagocytic lymphohistiocytosis (HLH), and some autho
85 2) inhibitor ruxolitinib in murine models of hemophagocytic lymphohistiocytosis (HLH), and the HLH-si
86 t spontaneously develop clinical features of hemophagocytic lymphohistiocytosis (HLH), but do so when
87 ne have been described in some patients with hemophagocytic lymphohistiocytosis (HLH), but the role o
88 led to the life-threatening immune disorder hemophagocytic lymphohistiocytosis (HLH), characterized
90 oss of normal immune regulation and underlie hemophagocytic lymphohistiocytosis (HLH), which requires
91 Here, we characterize 2 novel monoallelic hemophagocytic lymphohistiocytosis (HLH)-associated muta
99 irms the occurrence of reversible AKI due to hemophagocytic lymphohistiocytosis-induced activated mac
105 ncluding fulminant infectious mononucleosis, hemophagocytic lymphohistiocytosis, lymphoproliferative
107 sttransplant plasma cell hepatitis, familial hemophagocytic lymphohistiocytosis, pediatric nonalcohol
110 ed lymphomas, lymphoproliferative disorders, hemophagocytic lymphohistiocytosis, solid tumors, and ot
111 n between macrophage activation syndrome and hemophagocytic lymphohistiocytosis still remain to be de
112 sociated with macrophage activation syndrome/hemophagocytic lymphohistiocytosis, such as interleukin
113 anatory mechanisms, possibly integrated into hemophagocytic lymphohistiocytosis syndrome, of infectio
115 ead to a spectrum of diseases, from familial hemophagocytic lymphohistiocytosis to an increased risk
117 Munc13-4, the mutation of which in familial hemophagocytic lymphohistiocytosis type 3 results in a p
120 n-knockout mouse strains and from a Familial Hemophagocytic Lymphohistiocytosis type 4 (FHL4) patient
121 ients with STX11 deficiency develop familial hemophagocytic lymphohistiocytosis type 4 (FHL4), a life
123 Recent analysis of patients with familial hemophagocytic lymphohistiocytosis type 5 has identified
124 atal immune dysregulation disorder, familial hemophagocytic lymphohistiocytosis (type 2 FHL, FHL2).
125 Similarly, treating children with familial hemophagocytic lymphohistiocytosis using reduced intensi
126 he perforin gene have been found in familial hemophagocytic lymphohistiocytosis, which shares some fe
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