Abo Bibliothek: Guest
Digitales Portal Digitale Bibliothek eBooks Zeitschriften Referenzen und Berichte Forschungssammlungen
Critical Reviews™ in Immunology
Impact-faktor: 1.404 5-jähriger Impact-Faktor: 3.347 SJR: 0.706 SNIP: 0.55 CiteScore™: 2.19

ISSN Druckformat: 1040-8401
ISSN Online: 2162-6472

Volumen 40, 2020 Volumen 39, 2019 Volumen 38, 2018 Volumen 37, 2017 Volumen 36, 2016 Volumen 35, 2015 Volumen 34, 2014 Volumen 33, 2013 Volumen 32, 2012 Volumen 31, 2011 Volumen 30, 2010 Volumen 29, 2009 Volumen 28, 2008 Volumen 27, 2007 Volumen 26, 2006 Volumen 25, 2005 Volumen 24, 2004 Volumen 23, 2003 Volumen 22, 2002 Volumen 21, 2001 Volumen 20, 2000 Volumen 19, 1999 Volumen 18, 1998 Volumen 17, 1997 Volumen 16, 1996 Volumen 15, 1995 Volumen 14, 1994

Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v26.i1.40
pages 81-96

Immune Defects in Fanconi Anemia

Sara R. Fagerlie
Fred Hutchinson Cancer Research Center, Clinical Research Division, Transplantation Biology Program, Seattle, WA
Grover C. Bagby
The Division of Hematology and Medical Oncology, Department of Medicine, The Oregon Health & Science University (OHSU) Cancer Institute; The Portland Veterans Affairs Medical Center, Portland, OR


Fanconi anemia (FA) is a genetic disorder characterized by sensitivity to DNA cross-linking agents, multiple congenital anomalies, progressive bone marrow failure, and an increased prevalence of malignancy. The nature of chromosomal instability in FA is better understood today than in the past, but the molecular pathogenesis of bone marrow failure in this disease has not been clarified. Although there is documented evidence that FA hematopoietic stem cells (HSC) have inherent defects that reduce their survival, the potential influence of auxiliary cells on the ability of the FA bone marrow microenvironment to maintain and support HSC in unknown. Historically, FA has not been represented as a disease that affects the lymphoid compartment. In this article we review the results of studies that suggest that the FA immune system is dysfunctional and may contribute to the pathogenesis of both FA bone marrow failure and neoplastic disease.

Articles with similar content:

Cell Fusion in Myeloma Marrow Microenvironment: Role in Tumor Progression
Critical Reviews™ in Oncogenesis, Vol.18, 2013, issue 1-2
Franco Dammacco, Franco Silvestris, Mauro Cives, Sabino Ciavarella
Proteoglycan-Induced Arthritis: Immune Regulation, Cellular Mechanisms, and Genetics
Critical Reviews™ in Immunology, Vol.23, 2003, issue 3
Tibor T. Glant, Alison Finnegan, Katalin Mikecz
Extracellular Vesicles as Potential Mediators of Epigenetic Reprogramming
Onco Therapeutics, Vol.6, 2015, issue 3-4
Anna Lewandowska Ronnegren
Autoimmune Etiology in Chronic Prostatitis Syndrome: An Advance in the Understanding of This Pathology
Critical Reviews™ in Immunology, Vol.27, 2007, issue 1
Virginia Elena Rivero, Ruben Dario Motrich, Clelia Maria Riera, Mariana Maccioni
Role of Bone Regeneration and Turnover Modulators in Control of Fracture
Critical Reviews™ in Eukaryotic Gene Expression, Vol.17, 2007, issue 3
Shimon Meretyk, Dina Lewinson, Michael Soudry, Nimrod Rozen, Tova Bick