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1 dysfunctional, resembling pulmonary alveolar proteinosis.
2 herosclerotic lesions and pulmonary alveolar proteinosis.
3 patients with idiopathic pulmonary alveolar proteinosis.
4 actant clearance, causing pulmonary alveolar proteinosis.
5 olated from patients with pulmonary alveolar proteinosis.
6 ore represent a recurrent mutation in lipoid proteinosis.
7 or to the pathogenesis of pulmonary alveolar proteinosis.
8 st common sites for ECM1 mutations in lipoid proteinosis.
9 nflammation leading to fibrosis and alveolar proteinosis.
10 nic inflammation, and two had focal alveolar proteinosis.
11 ng function that prevents pulmonary alveolar proteinosis.
12 ventilatory defects 63%, pulmonary alveolar proteinosis 18%, pulmonary arterial hypertension 9%), de
13 studied 12 subjects with pulmonary alveolar proteinosis, 61 healthy control subjects, and 12 control
14 disorder similar to human pulmonary alveolar proteinosis, a rare disease with congenital, infantile,
16 ar macrophages, thereby underlying pulmonary proteinosis and airborne infections, type I interferon v
17 t GM-CSF signaling caused pulmonary alveolar proteinosis and excessive IL-6 signaling promoted bone m
18 impaired in patients with pulmonary alveolar proteinosis and that GM-CSF autoantibodies cause the dys
19 e, cigarette smoking, and pulmonary alveolar proteinosis and the implications of obesity and obstruct
22 lerosis, type 2 diabetes, pulmonary alveolar proteinosis, and obesity, have a chronic inflammatory co
23 ssion profile of a variant causal for lipoid proteinosis, and with a simulation study to assess our m
25 s against GM-CSF underlie pulmonary alveolar proteinosis; associated infections are less well charact
26 h failure, renal disease, pulmonary alveolar proteinosis, autoimmune disorders and osteoporosis, are
29 crine syndrome type I and pulmonary alveolar proteinosis, detecting ACAA levels consistent with those
30 pe of decreased GM-CSF function is pulmonary proteinosis due to aberrant function of alveolar macroph
31 respiratory infections and develop alveolar proteinosis due to defects in innate immune function and
33 d cell debris in airways (pulmonary alveolar proteinosis) due to impaired development of alveolar mac
35 ophils from subjects with pulmonary alveolar proteinosis had normal ultrastructure and differentiatio
37 r identical to hereditary pulmonary alveolar proteinosis (hPAP) in children with CSF2RA or CSF2RB mut
39 al and prevented the development of alveolar proteinosis in mice transplanted with GM-Csf-receptor-de
41 ronic interstitial inflammation and alveolar proteinosis, inflammation of the glandular stomach and s
44 ice lacking beta c show a pulmonary alveolar proteinosis-like disease and reduced numbers of peripher
46 uman SP-A (isolated from normal and alveolar proteinosis lungs) and SP-D (recombinant protein and pro
48 itis obliterans (n = 21), pulmonary alveolar proteinosis (n = 12), pulmonary fibrosis (n = 15), and o
49 ccupational burden, 30%); pulmonary alveolar proteinosis (occupational burden, 29%); tuberculosis (oc
50 nfection in patients with pulmonary alveolar proteinosis occurs in association with high levels of au
51 B, and C in lavage fluids from patients with proteinosis of different causes in comparison with healt
52 for later development of pulmonary alveolar proteinosis or other opportunistic infections, and that
53 impaired in patients with pulmonary alveolar proteinosis, owing to the presence of GM-CSF autoantibod
54 t it is elevated in human pulmonary alveolar proteinosis (PAP) and in the GM-CSF knockout mouse, a mu
70 upus erythematosus (SLE), pulmonary alveolar proteinosis (PAP) or multiple sclerosis) and coronavirus
72 dies are thought to cause pulmonary alveolar proteinosis (PAP), a rare syndrome characterized by myel
73 phy is characteristic for pulmonary alveolar proteinosis (PAP), it is not specific and has not been c
74 independent kindreds have pulmonary alveolar proteinosis (PAP), progressive polycystic lung disease,
75 how its disruption causes pulmonary alveolar proteinosis (PAP), we evaluated lipid composition in alv
79 a slightly more severe mucocutaneous lipoid proteinosis phenotype, but neurological features do not
84 in 10 further unrelated patients with lipoid proteinosis to extend genotype-phenotype correlation and
85 unction characteristic of pulmonary alveolar proteinosis was reproduced in a dose-dependent fashion i
86 larities between lichen sclerosus and lipoid proteinosis, which results from mutations in extracellul
88 Five patients developed pulmonary alveolar proteinosis without mutations in the granulocyte-macroph