DOCK8 and STAT3 dependent inhibition of IgE isotype switching by TLR9 ligation in human B cells.
Massaad, Michel J; Cangemi, Brittney; Al-Herz, Waleed; LeFranc, Gérard; Freeman, Alexandra; Baxi, Sachin; Keles, Sevgi; Metin, Ayse; Dasouki, Majid; Sobh, Ali; Kanariou, Maria; Al-Sukaiti, Nashat; Ozen, Ahmet; Ochs, Hans; Chatila, Talal A; Manis, John P; Geha, Raif.
; 183: 263-265, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28882618
DOCK8 functions as an adaptor that links TLR-MyD88 signaling to B cell activation.
Dedicator of cytokinesis 8 regulates signal transducer and activator of transcription 3 activation and promotes T17 cell differentiation.
Hypomorphic function and somatic reversion of DOCK8 cause combined immunodeficiency without hyper-IgE.
Expansion of CCR4+ activated T cells is associated with memory B cell reduction in DOCK8-deficient patients.
El monocito/macrófago como diana terapéutica en la aterosclerosis
The first cohort of Iranian patients with hyper immunoglobulin E syndrome: A long-term follow-up and genetic analysis.
The extended clinical phenotype of 64 patients with dedicator of cytokinesis 8 deficiency.