[1] 桂永浩, 薛辛东.儿科学[M]. 3版. 北京:人民卫生出版社,2015:470-471. [2] Casanova JL, Beaucoudrey LD, Puel A, et al. Mutations in STAT3 and IL12RB1 impair the development of human IL-17-producing T cells[J]. J Exp Med,2008,205(7):1543-1550. [3] Ma CS, Chew GY, Simpson N, et al. Deficiency of Th17 cells in hyper-IgE syndrome due to mutations in STAT3[J]. J Exp Med,2008,205(7):1551-1557. [4] Chang Y, Kang SY, Kim J, et al. Functional defects in type 3 innate lymphoid cells and classical monocytes in a patient with hyper-IgE syndrome[J]. Immune Netw,2017,17(5): 352-364. [5] Engelhardt KR, McGhee S, Winkler S, et al. Large deletions and point mutations involving DOCK8 in the autosomal recessive form of the hyper-IgE syndrome[J]. J Allergy Clin Immunol, 2009,124(6):1289-1295. [6] Kearney CJ,Vervoort SJ, Ramsbottom KM, et al. DOCK8 drives Src-dependent NK cell effector function[J]. J Immunol, 2017,199(6):751-757. [7] Yang L,Fliegauf M, Grimbacher B. Hyper-IgE syndromes: reviewing PGM3 deficiency[J]. Curr Opin Pediatr,2014,26(6):697-703. [8] VSzczawinska-Poplonyk A, Kycler Z, Pietrucha B, et al. The hyperimmunoglobulin E syndrome-clinical manifestation diversity in primary immune deficiency[J]. Orphanet J Rare Dis,2011,6(1):76-87. [9] Sasihuseyinoglu AS, Yilmaz M, Altintas DU, et al. Squamous cell carcinoma with hyper-IgE syndrome: a case report[J]. J Pediatr Hematol Oncol, 2017,1(2):95-103. [10] Woellner C, Gertz EM, Schäffer AA, et al. Mutations in STAT3 and diagnostic guidelines for hyper-IgE syndrome[J]. J Allergy Clin Immunol,2010,125(2):424-432. [11] Grimbacher B, Holland SM, Gallin JI, et al. Hyper-IgE syndrome with recurrent infections-an autosomal dominant multisystem disorder[J]. N Engl J Med,1999, 340(9): 692-702. [12] Minegishi Y, Karasuyama H. Hyperimmunoglobulin E syndrome and tyrosine kinase 2 deficiency[J]. Curr Opin Allergy Clin Immunol,2007,7(6):506-509. [13] Hagl B, Heinz V, Schlesinger A, et al. Key findings to expedite the diagnosis of hyper-IgE syndromes in infants and young children[J]. Pediatr Allergy Immunol,2016,27(2):177-184. [14] Grimbacher B, Schaffer AA, Holland SM, et al. Genetic linkage of hyper-IgE syndrome to chromosome 4[J]. Am J Hum Genet,1999,65(3):735-744. [15] Kumanovics A, Wittwer CT, Pryor RJ, et al. Rapid molecular analysis of the STAT3 gene in job sndrome of Hyper-IgE and recurrent infectious diseases[J]. J Mol Diagn,2010,12(2):213-219. [16] Engelhardt KR, Gertz ME, Keles S, et al.The extended clinical phenotype of 64 patients with dedicator of cytokinesis 8 deficiency[J]. J Allergy Clin Immunol,2015,136(2):402-412. [17] Vogel TP, Milner JD, Cooper MA.The Ying and Yang of STAT3 in human disease[J]. J Clin Immunol,2015,35(7):615-623. [18] DeWitt CA, Bishop AB, Buescher LS, et al. Hyperimmunoglobulin E syndrome: Two cases and a review of the literature[J]. J Am Acad Dermatol,2006,54(5):855-865. [19] Hashemi H, Mohebbi M, Mehravaran S, el al. Hyperamoglobulin E syndrome: Genetics, immunopathies, clinical findings and treatment[J]. J Res Med Sci,2017,22(3),53-60. [20] Uygun DFK, Uygun V, Reisli l, et al. Hematopoietic stem cell transplantation from unrelated donors in children with DOCK8[J]. Pediatric Transplantation,2017,21(7):402-411. [21] Casale TB. Anti-immunoglobulin E (omalizumab) therapy in seasonal allergic rhinitis[J]. Am J Respir Crit Care Med,2001,164(8Pt2):18-21.
PDF(610 KB)
