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1 entiation (STAT3, STAT1, CARD9) are prone to mucocutaneous candidiasis.
2 hreatening autoimmune cytopenias and chronic mucocutaneous candidiasis.
3 owever, they still had infections, including mucocutaneous candidiasis.
4 1 (STAT1) have been associated with chronic mucocutaneous candidiasis.
5 Four patients had recurrent mucocutaneous candidiasis.
6 t linkage assignment of a dominant locus for mucocutaneous candidiasis.
7 dism, autoimmune adrenocortical failure, and mucocutaneous candidiasis.
8 iseases, including invasive tuberculosis and mucocutaneous candidiasis.
9 d clinical manifestations, including chronic mucocutaneous candidiasis, AI, and asplenia, respectivel
11 ator of transcription 1 (STAT1) with chronic mucocutaneous candidiasis and PML was reported previousl
12 linkage region on chromosome 2p for chronic mucocutaneous candidiasis and thyroid disease, previousl
13 matoceles, eczema, staphylococcal abscesses, mucocutaneous candidiasis, and abnormalities of bone and
14 ponses, improved TH17 differentiation, cured mucocutaneous candidiasis, and maintained remission of i
15 rized by multiple endocrine failure, chronic mucocutaneous candidiasis, and various ectodermal defect
16 in IL17F and IL17R in patients with chronic mucocutaneous candidiasis, as well as neutralizing autoa
17 mutations have been associated with chronic mucocutaneous candidiasis, but the role of CARD9 in inte
18 eficiency in mice or humans leads to chronic mucocutaneous candidiasis, but the specific downstream m
21 have recently been shown to underlie chronic mucocutaneous candidiasis (CMC), while inborn errors of
25 ial disease (hypomorphic alleles) to chronic mucocutaneous candidiasis (CMC; hypermorphic alleles).
26 rent bacterial infections, viral infections, mucocutaneous candidiasis, cutaneous warts, and skin abs
27 cells; meanwhile, some patients with chronic mucocutaneous candidiasis disease might also have viral
30 rge family in which a combination of chronic mucocutaneous candidiasis (fungal infections of the skin
32 autoimmune disorder characterized by chronic mucocutaneous candidiasis, hypoparathyroidism, and adren
33 pecies infection, Norwegian scabies, chronic mucocutaneous candidiasis, hypothyroidism, and esophagea
34 nti-IL-17F, or anti-IL-22 autoantibodies and mucocutaneous candidiasis in the setting of either APECE
35 ciency (AI), hypoparathyroidism, and chronic mucocutaneous candidiasis plus autoantibodies neutralizi
37 ients with unusual susceptibility to chronic mucocutaneous candidiasis resulting from T(H)17 deficien
38 nt, both subjects with mosaicism had chronic mucocutaneous candidiasis, suggesting that candidiasis i
39 risingly, it is also associated with chronic mucocutaneous candidiasis, through as yet undetermined m
42 -17A and interleukin-17F (IL-17A/F) underlie mucocutaneous candidiasis, whereas inborn errors of inte
43 utations, including recurrent infections and mucocutaneous candidiasis, which are suggestive of TH17
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