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1 entiation (STAT3, STAT1, CARD9) are prone to mucocutaneous candidiasis.
2 owever, they still had infections, including mucocutaneous candidiasis.
3 1 (STAT1) have been associated with chronic mucocutaneous candidiasis.
4 Four patients had recurrent mucocutaneous candidiasis.
5 t linkage assignment of a dominant locus for mucocutaneous candidiasis.
6 dism, autoimmune adrenocortical failure, and mucocutaneous candidiasis.
7 nic bacterial diseases and interleukin-17A/F mucocutaneous candidiasis.
8 hreatening autoimmune cytopenias and chronic mucocutaneous candidiasis.
9 s for immunodeficiency patients with chronic mucocutaneous candidiasis.
10 iseases, including invasive tuberculosis and mucocutaneous candidiasis.
11 d clinical manifestations, including chronic mucocutaneous candidiasis, AI, and asplenia, respectivel
13 Most patients present with severe chronic mucocutaneous candidiasis and organ-specific autoimmunit
14 ator of transcription 1 (STAT1) with chronic mucocutaneous candidiasis and PML was reported previousl
16 -17A/F and IL-6 are less common and underlie mucocutaneous candidiasis and staphylococcal diseases, r
17 linkage region on chromosome 2p for chronic mucocutaneous candidiasis and thyroid disease, previousl
18 matoceles, eczema, staphylococcal abscesses, mucocutaneous candidiasis, and abnormalities of bone and
19 ponses, improved TH17 differentiation, cured mucocutaneous candidiasis, and maintained remission of i
20 rized by multiple endocrine failure, chronic mucocutaneous candidiasis, and various ectodermal defect
21 in IL17F and IL17R in patients with chronic mucocutaneous candidiasis, as well as neutralizing autoa
22 mutations have been associated with chronic mucocutaneous candidiasis, but the role of CARD9 in inte
23 eficiency in mice or humans leads to chronic mucocutaneous candidiasis, but the specific downstream m
24 NCL-EPO-NPs also significantly abrogated mucocutaneous candidiasis by fluconazole-resistant strai
25 tor (AIRE) mutations, manifests with chronic mucocutaneous candidiasis (CMC) and multisystem autoimmu
28 in humans have been associated with chronic mucocutaneous candidiasis (CMC), as well as with increas
29 have recently been shown to underlie chronic mucocutaneous candidiasis (CMC), while inborn errors of
33 ial disease (hypomorphic alleles) to chronic mucocutaneous candidiasis (CMC; hypermorphic alleles).
34 rent bacterial infections, viral infections, mucocutaneous candidiasis, cutaneous warts, and skin abs
35 cells; meanwhile, some patients with chronic mucocutaneous candidiasis disease might also have viral
38 rge family in which a combination of chronic mucocutaneous candidiasis (fungal infections of the skin
40 lyendocrine syndrome type-1 (APS-1), chronic mucocutaneous candidiasis has been ascribed to neutraliz
41 autoimmune disorder characterized by chronic mucocutaneous candidiasis, hypoparathyroidism, and adren
42 pecies infection, Norwegian scabies, chronic mucocutaneous candidiasis, hypothyroidism, and esophagea
44 nti-IL-17F, or anti-IL-22 autoantibodies and mucocutaneous candidiasis in the setting of either APECE
46 ciency (AI), hypoparathyroidism, and chronic mucocutaneous candidiasis plus autoantibodies neutralizi
48 ients with unusual susceptibility to chronic mucocutaneous candidiasis resulting from T(H)17 deficien
49 suffer from cold staphylococcal lesions and mucocutaneous candidiasis, severe allergy, and skeletal
50 nt, both subjects with mosaicism had chronic mucocutaneous candidiasis, suggesting that candidiasis i
51 17F.S65L) was identified that causes chronic mucocutaneous candidiasis, suggesting the existence of e
52 risingly, it is also associated with chronic mucocutaneous candidiasis, through as yet undetermined m
55 -17A and interleukin-17F (IL-17A/F) underlie mucocutaneous candidiasis, whereas inborn errors of inte
56 utations, including recurrent infections and mucocutaneous candidiasis, which are suggestive of TH17
57 describe 2 patients presenting with chronic mucocutaneous candidiasis who harbor biallelic nonsense