The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Deficient T Cell Receptor Excision Circles (TRECs) in autosomal recessive hyper IgE syndrome caused by DOCK8 mutation: Implications for pathogenesis and potential detection by newborn screening
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“Several mutations affecting actin remodeling have been implicated in T-cell lymphopenia, including cofilin (Cfl1), 40 coronin 1a (CORO1A), 41 Dock8, 42 WASp (WAS), 43 and ARPC1B, 44 each affecting thymocyte development differently.”
From Dominant activating RAC2 mutation with lymphopenia, immunodeficiency, and cytoskeletal defects (2019) · cites this paper as [42]
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Cites
Changes in thymic function with age and during the treatment of HIV infection
Douek, D. C., McFarland, R. D., Keiser, P. H., Gage, E. A., Massey, J. M., Haynes, B. F., Polis, M. A., Haase, A. T., Feinberg, M. B., Sullivan#, J. L., et al. (1998) · Nature · doi:10.1038/25374 · Cited by 1,893
Research works printed but not linked: 21
- Renner, 2004, Autosomal Recessive Hyperimmunoglobulin E Syndrome: A distinct disease entity, J. Pediatr., 144, 93, 10.1016/S0022-3476(03)00449-9 · DOI
- Grimbacher, 1999, Hyper-IgE syndrome with recurrent infections—an autosomal dominant multisystem disorder, N. Engl. J. Med., 340, 692, 10.1056/NEJM199903043400904 · DOI
- Minegishi, 2007, Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome, Nature, 448, 1058, 10.1038/nature06096 · DOI
- Holland, 2007, STAT3 mutations in the hyper-IgE syndrome, N. Engl. J. Med., 357, 1608, 10.1056/NEJMoa073687 · DOI
- Al Khatib, 2009, Defects along the T(H)17 differentiation pathway underlie genetically distinct forms of the hyper IgE syndrome, Allergy Clin. Immunol., 124, 342, 10.1016/j.jaci.2009.05.004 · DOI
- Zhang, 2009, Combined immunodeficiency associated with DOCK8 mutations, N. Engl. J. Med., 361, 2046, 10.1056/NEJMoa0905506 · DOI
- Engelhardt, 2009, Large deletions and point mutations involving the dedicator of cytokinesis 8 (DOCK8) in the autosomal-recessive form of hyper-IgE syndrome, J. Allergy Clin. Immunol., 124, 1289, 10.1016/j.jaci.2009.10.038 · DOI
- Gatz, 2010, Curative treatment of autosomal-recessive hyper-IgE syndrome by hematopoietic cell transplantation, Bone Marrow Transplant., 1
- Bittner, 2010, Successful long-term correction of autosomal recessive hyper-IgE syndrome due to DOCK8 deficiency by hematopoietic stem cell transplantation, Klin. Padiatr., 222, 351, 10.1055/s-0030-1265135 · DOI
- McDonald, 2010, Successful engraftment of donor marrow after allogeneic hematopoietic cell transplantation in autosomal-recessive hyper-IgE syndrome caused by dedicator of cytokinesis 8 deficiency, J. Allergy Clin. Immunol., 126, 1304, 10.1016/j.jaci.2010.07.034 · DOI
- Grimbacher, 1999, Genetic Linkage of Hyper-IgE Syndrome to Chromosome 4, Am. J. Hum. Genet., 65, 735, 10.1086/302547 · DOI
- Chan, 2005, Development of population-based newborn screening for severe combined immunodeficiency, J. Allergy Clin. Immunol., 115, 391, 10.1016/j.jaci.2004.10.012 · DOI
- Pien, 2008, Evaluation and clinical interpretation of hypergammaglobulinemia E: differentiating atopy from immunodeficiency, Ann. Allergy Asthma Immunol., 100, 392, 10.1016/S1081-1206(10)60605-9 · DOI
- Meller, 2005, CZH proteins: a new family of Rho-GEFs, J. Cell Sci., 118, 4937, 10.1242/jcs.02671 · DOI
- Cote, 2007, GEF what? Dock180 and related proteins help Rac to polarize cells in new ways, Trends Cell. Biol., 17, 383, 10.1016/j.tcb.2007.05.001 · DOI
- Randall, 2009, Dock8 mutations cripple B cell immunological synapses, germinal centers and long-lived antibody production, Nat. Immunol., 10, 1283, 10.1038/ni.1820 · DOI
- Minegishi, 2006, Human tyrosine kinase 2 deficiency reveals its requisite roles in multiple cytokine signals involved in innate and acquired immunity, Immunity, 25, 745, 10.1016/j.immuni.2006.09.009 · DOI
- Puck, 2007, Neonatal screening for severe combined immune deficiency, Curr. Opin. Allergy Clin. Immunol., 7, 522, 10.1097/ACI.0b013e3282f14a2a · DOI
- Routes, 2009, Statewide Newborn Screening for Severe T-Cell Lymphopenia, JAMA, 302, 2465, 10.1001/jama.2009.1806 · DOI · Paper page
- Gerstel-Thompson, 2010, High-Throughput Multiplexed T-Cell–Receptor Excision Circle Quantitative PCR Assay with Internal Controls for Detection of Severe Combined Immunodeficiency in Population-Based Newborn Screening, Clin. Chem., 56, 1466, 10.1373/clinchem.2010.144915 · DOI
- Janik, 2010, A Multiplex Immunoassay Using the Guthrie Specimen to Detect T-Cell Deficiencies Including Severe Combined Immunodeficiency Disease, Clin. Chem., 56, 1460, 10.1373/clinchem.2010.144329 · DOI
Cited by
RHO GTPases: from new partners to complex immune syndromes
El Masri, R., & Delon, J. (2021) · Nature Reviews Immunology · doi:10.1038/s41577-021-00500-7 · Cited by 131
Dominant activating RAC2 mutation with lymphopenia, immunodeficiency, and cytoskeletal defects
Hsu, A. P., Donkó, A., Arrington, M. E., Swamydas, M., Fink, D., Das, A., Escobedo, O., Bonagura, V., Szabolcs, P., Steinberg, H. N., et al. (2019) · Blood · doi:10.1182/blood-2018-11-886028 · Cited by 92
Metadata
- Authors
- Dasouki, M., Okonkwo, K. C., Ray, A., Folmsbeel, C. K., Gozales, D., Keles, S., Puck, J. M., & Chatila, T.
- Venue
- Clinical Immunology
- Publisher
- Elsevier BV
- Published
- 2011-11
- Volume
- 141
- Issue
- 2
- Pages
- 128-132
- ISSN
- 1521-6616
- PMC
- PMC4210456
- Cited by
- 58
- References
- 1
- Language
- en
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- CoChat. (2026). Citation check: Deficient T Cell Receptor Excision Circles (TRECs) in autosomal recessive hyper IgE syndrome caused by DOCK8 mutation: Implications for pathogenesis and potential detection by newborn screening. https://app.cochat.ai/papers/10.1016/j.clim.2011.06.003
- The paper
- Dasouki, M., Okonkwo, K. C., Ray, A., Folmsbeel, C. K., Gozales, D., Keles, S., Puck, J. M., & Chatila, T. (2011). Deficient T Cell Receptor Excision Circles (TRECs) in autosomal recessive hyper IgE syndrome caused by DOCK8 mutation: Implications for pathogenesis and potential detection by newborn screening. Clinical Immunology. https://doi.org/10.1016/j.clim.2011.06.003
