A Durandy

Summary

Country: France

Publications

  1. ncbi request reprint Activation-induced cytidine deaminase: structure-function relationship as based on the study of mutants
    Anne Durandy
    Institut National de la Sante et de la Recherche Medicale INSERM, U768, Hopital Necker Enfants Malades, Paris, France
    Hum Mutat 27:1185-91. 2006
  2. ncbi request reprint Anti-B cell and anti-cytokine therapy for the treatment of post-transplant lymphoproliferative disorder: past, present, and future
    A Durandy
    INSERM U429, Hôpital Necker 149 rue de Sèvres 75075 Paris, France
    Transpl Infect Dis 3:104-7. 2001
  3. ncbi request reprint Hyper-IgM syndromes: a model for studying the regulation of class switch recombination and somatic hypermutation generation
    A Durandy
    INSERM U429, Hopital Necker Enfants Malades, 149 rue de Sevres, Paris, France
    Biochem Soc Trans 30:815-8. 2002
  4. ncbi request reprint Genetically acquired class-switch recombination defects: the multi-faced hyper-IgM syndrome
    Melinda Erdos
    Department of Infectology and Pediatric Immunology, Medical and Health Science Centre, University of Debrecen, Debrecen, Hungary
    Immunol Lett 97:1-6. 2005
  5. ncbi request reprint Immunoglobulin replacement therapy in primary antibody deficiency diseases--maximizing success
    Anne Durandy
    Hopital Necker Enfants Malades, Paris, France
    Int Arch Allergy Immunol 136:217-29. 2005
  6. pmc A primary immunodeficiency characterized by defective immunoglobulin class switch recombination and impaired DNA repair
    Sophie Peron
    Institut National de la Sante et de la Recherche Medicale, U768, Paris, France
    J Exp Med 204:1207-16. 2007
  7. ncbi request reprint Terminal defects of B lymphocyte differentiation
    A Durandy
    INSERM U429, Hopital Necker Enfants Malades, Paris, France
    Curr Opin Allergy Clin Immunol 1:519-24. 2001
  8. ncbi request reprint Hyper-immunoglobulin-M syndromes caused by an intrinsic B cell defect
    Anne Durandy
    INSERM U429, Hospital Necker Sick Children, Paris, France
    Curr Opin Allergy Clin Immunol 3:421-5. 2003
  9. ncbi request reprint [Development of specific immunity in prenatal life]
    A Durandy
    INSERM U429, Hopital Necker Enfants Malades, 149, rue de Sevres, 75015 Paris, France
    Arch Pediatr 8:979-85. 2001
  10. ncbi request reprint Human genetic defects in class-switch recombination (hyper-IgM syndromes)
    A Durandy
    Institut National de la Santé et de la Recherche Médicale INSERM U429, Hopital Necker Enfants Malades, 149 rue de Sevres, Cedex 15, Paris, France
    Curr Opin Immunol 13:543-8. 2001

Detail Information

Publications57

  1. ncbi request reprint Activation-induced cytidine deaminase: structure-function relationship as based on the study of mutants
    Anne Durandy
    Institut National de la Sante et de la Recherche Medicale INSERM, U768, Hopital Necker Enfants Malades, Paris, France
    Hum Mutat 27:1185-91. 2006
    ....
  2. ncbi request reprint Anti-B cell and anti-cytokine therapy for the treatment of post-transplant lymphoproliferative disorder: past, present, and future
    A Durandy
    INSERM U429, Hôpital Necker 149 rue de Sèvres 75075 Paris, France
    Transpl Infect Dis 3:104-7. 2001
    ..Because IL6 has been described as a growth factor for EBV-infected B cells, anti-IL6 monoclonal antibody therapy was also tested in a phase I-II clinical trial, the results of which are summarized...
  3. ncbi request reprint Hyper-IgM syndromes: a model for studying the regulation of class switch recombination and somatic hypermutation generation
    A Durandy
    INSERM U429, Hopital Necker Enfants Malades, 149 rue de Sevres, Paris, France
    Biochem Soc Trans 30:815-8. 2002
    ....
  4. ncbi request reprint Genetically acquired class-switch recombination defects: the multi-faced hyper-IgM syndrome
    Melinda Erdos
    Department of Infectology and Pediatric Immunology, Medical and Health Science Centre, University of Debrecen, Debrecen, Hungary
    Immunol Lett 97:1-6. 2005
  5. ncbi request reprint Immunoglobulin replacement therapy in primary antibody deficiency diseases--maximizing success
    Anne Durandy
    Hopital Necker Enfants Malades, Paris, France
    Int Arch Allergy Immunol 136:217-29. 2005
    ....
  6. pmc A primary immunodeficiency characterized by defective immunoglobulin class switch recombination and impaired DNA repair
    Sophie Peron
    Institut National de la Sante et de la Recherche Medicale, U768, Paris, France
    J Exp Med 204:1207-16. 2007
    ..Overall, these findings suggest that a unique Ig CSR deficiency phenotype could be related to an as-yet-uncharacterized defect in a DNA repair pathway involved in both CSR and SHM events...
  7. ncbi request reprint Terminal defects of B lymphocyte differentiation
    A Durandy
    INSERM U429, Hopital Necker Enfants Malades, Paris, France
    Curr Opin Allergy Clin Immunol 1:519-24. 2001
    ....
  8. ncbi request reprint Hyper-immunoglobulin-M syndromes caused by an intrinsic B cell defect
    Anne Durandy
    INSERM U429, Hospital Necker Sick Children, Paris, France
    Curr Opin Allergy Clin Immunol 3:421-5. 2003
    ....
  9. ncbi request reprint [Development of specific immunity in prenatal life]
    A Durandy
    INSERM U429, Hopital Necker Enfants Malades, 149, rue de Sevres, 75015 Paris, France
    Arch Pediatr 8:979-85. 2001
    ..The various antigenic stimulations and T/B cell cooperations allow a complete maturation of the immune system during the first years of life...
  10. ncbi request reprint Human genetic defects in class-switch recombination (hyper-IgM syndromes)
    A Durandy
    Institut National de la Santé et de la Recherche Médicale INSERM U429, Hopital Necker Enfants Malades, 149 rue de Sevres, Cedex 15, Paris, France
    Curr Opin Immunol 13:543-8. 2001
    ....
  11. ncbi request reprint Hyper-IgM syndromes
    Anne Durandy
    Inserm U768, René Descartes Paris 5 University, France
    Curr Opin Rheumatol 18:369-76. 2006
    ..The recent elucidation of the molecular defects leading to hyper-IgM syndromes has provided considerable insight into the complex mechanisms that govern the antibody maturation in humans...
  12. ncbi request reprint Activation-induced cytidine deaminase: a dual role in class-switch recombination and somatic hypermutation
    Anne Durandy
    INSERM U429, Hopital Necker Enfants Malades, Paris, France
    Eur J Immunol 33:2069-73. 2003
    ..However, the immunological abnormalities observed in uracil-N glycosylase deficiency in a recent study indirectly suggest that AID may edit DNA directly...
  13. ncbi request reprint Hyper-immunoglobulin M syndromes caused by intrinsic B-lymphocyte defects
    Anne Durandy
    INSERM U429, Hopital Necker Enfants Malades, Paris, France
    Immunol Rev 203:67-79. 2005
    ..The mechanism of action of AID remains somewhat debated, but the observation that uracil-DNA-glycosylase deficiency leads to a severe hyper-IgM syndrome strongly argues in favor of a DNA-editing activity of AID...
  14. ncbi request reprint Abnormal CD40-mediated activation pathway in B lymphocytes from patients with hyper-IgM syndrome and normal CD40 ligand expression
    A Durandy
    INSERM Unit 429, Hospital Necker Enfants Malades, Paris, France
    J Immunol 158:2576-84. 1997
    ....
  15. ncbi request reprint CD40 ligand expression deficiency in a female carrier of the X-linked hyper-IgM syndrome as a result of X chromosome lyonization
    G de Saint Basile
    Unité de Recherches sur le dévelopement normal et pathologique du système immunitaire INSERM U 429, Hopital Necker Enfants Malades, Paris, France
    Eur J Immunol 29:367-73. 1999
    ..Therefore, it is possible that some cases of CVID in females represent partial deficiency of CD40L expression in carriers of the CD40L mutation...
  16. pmc Inherited interleukin 12 deficiency in a child with bacille Calmette-Guérin and Salmonella enteritidis disseminated infection
    F Altare
    INSERM U429, Hopital Necker Enfants Malades, Paris, France
    J Clin Invest 102:2035-40. 1998
    ..This is the first discovered human disease resulting from a cytokine gene defect. It suggests that IL-12 is essential to and appears specific for protective immunity to intracellular bacteria such as mycobacteria and salmonella...
  17. ncbi request reprint TGF-beta 1 prevents the noncognate maturation of human dendritic Langerhans cells
    F Geissmann
    Unité de Recherche Associée 1461, Centre National de la Recherche Scientifique, Institut National de la Sante et de la Recherche Medicale, Unite 429, Paris, France
    J Immunol 162:4567-75. 1999
    ..We conclude that TGF-beta 1 appears to be responsible for both the acquisition of LC phenotype, cytokine production pattern, and prevention of noncognate maturation...
  18. pmc Hyper-IgM syndrome type 4 with a B lymphocyte-intrinsic selective deficiency in Ig class-switch recombination
    Kohsuke Imai
    Institut National de la Santé et de la Recherche Médicale INSERM U429, Hopital Necker Enfants Malades, Paris, France
    J Clin Invest 112:136-42. 2003
    ..Thus, HIGM4 is probably the consequence of a selective defect either in a CSR-specific factor of the DNA repair machinery or in survival signals delivered to switched B cells...
  19. ncbi request reprint Activation-induced cytidine deaminase (AID) deficiency causes the autosomal recessive form of the Hyper-IgM syndrome (HIGM2)
    P Revy
    INSERM U429, Hopital Necker Enfants Malades, Paris, France
    Cell 102:565-75. 2000
    ..The phenotype observed in HIGM2 patients (and in AID-/- mice) demonstrates the absolute requirement for AID in several crucial steps of B cell terminal differentiation necessary for efficient antibody responses...
  20. ncbi request reprint Epidermal Langerhans' cells in children with primary T-cell immune deficiencies
    J F Emile
    Service d Anatomie et de Cytologie Pathologiques, Hopital Necker Enfants Malades, Paris, France
    J Pathol 183:70-4. 1997
    ..By contrast, no LC were detected in the skin samples of two children with alymphocytosis and of a child with reticular dysgenesis, a condition characterized by the absence of peripheral blood leukocytes...
  21. ncbi request reprint Inherited defects of immunoglobulin class switch recombination
    Sven Kracker
    INSERM, U768 Université Paris Descartes, Faculté de Médecine René Descartes, Paris, F 75005, France
    Adv Exp Med Biol 685:166-74. 2010
    ..Novel findings are awaited from the study ofyet-genetically undefined CSR-deficiencies, probably leading to the identification of AID cofactor(s) and/or proteins involved in CSR-induced DNA repair...
  22. ncbi request reprint X-linked anhidrotic ectodermal dysplasia with immunodeficiency is caused by impaired NF-kappaB signaling
    R Doffinger
    Laboratoire de Genetique Humaine des Maladies Infectieuses, Faculte de Medecine Necker Enfants Malades, Paris, France
    Nat Genet 27:277-85. 2001
    ..We thus report for the first time that impaired but not abolished NF-kappaB signaling in humans results in two related syndromes that associate specific developmental and immunological defects...
  23. ncbi request reprint The block in immunoglobulin class switch recombination caused by activation-induced cytidine deaminase deficiency occurs prior to the generation of DNA double strand breaks in switch mu region
    Nadia Catalan
    Institut National de la Sante et de la Recherche Medicale, Unite 429, Hopital Necker Enfants Malades, 149 rue de Sevres, 75015 Paris, France
    J Immunol 171:2504-9. 2003
    ....
  24. ncbi request reprint Analysis of class switch recombination and somatic hypermutation in patients affected with autosomal dominant hyper-IgM syndrome type 2
    Kohsuke Imai
    Institut National de la Santé et de la Recherche Médicale INSERM Unité 429, Hopital Necker Enfants Malades, Paris, France
    Clin Immunol 115:277-85. 2005
    ..The characteristics of the AD-HIGM2 phenotype indicate that the AID C-terminal region may be involved in DNA repair machinery required for CSR...
  25. ncbi request reprint Activation of the Janus kinase 3-STAT5a pathway after CD40 triggering of human monocytes but not of resting B cells
    P Revy
    Institut National de la Sante et de la Recherche Medicale, Unite 429, Hopital Necker Enfants Malades, Paris, France
    J Immunol 163:787-93. 1999
    ..This observation is consistent with the detection of normal CD40-induced monocyte activation in patients with CD40 ligand+ hyper IgM syndrome in whom a defect in CD40-induced B cell activation has been reported...
  26. ncbi request reprint Human models of inherited immunoglobulin class switch recombination and somatic hypermutation defects (hyper-IgM syndromes)
    Anne Durandy
    INSERM U429, Hopital Necker Enfants Malades, 75015 Paris, France
    Adv Immunol 82:295-330. 2004
  27. pmc Control of human B cell tumor growth in severe combined immunodeficiency mice by monoclonal anti-B cell antibodies
    A Durandy
    Institut National de la Sante et de la Recherche Medicale, U 132, Hopital des Enfants Malades, Paris, France
    J Clin Invest 90:945-52. 1992
    ..These results indicate that scid mice may be suitable for assessing therapeutic approaches to human B cell proliferation...
  28. doi request reprint Immunoglobulin class switch recombination deficiencies
    S Kracker
    INSERM, U768, Hopital Necker Enfants Malades, Universite Paris Descartes, Faculté de Médecine Paris V René Descartes, Paris F 75005, France
    Clin Immunol 135:193-203. 2010
    ....
  29. ncbi request reprint Cernunnos, a novel nonhomologous end-joining factor, is mutated in human immunodeficiency with microcephaly
    Dietke Buck
    INSERM, Hopital Necker Enfants Malades, U768 Unité Développement Normal et Pathologique du Système Immunitaire, Paris, France
    Cell 124:287-99. 2006
    ..All five patients carry mutations in the Cernunnos gene, which was identified through cDNA functional complementation cloning. Cernunnos/XLF represents a novel DNA repair factor essential for the NHEJ pathway...
  30. pmc Retinoids regulate survival and antigen presentation by immature dendritic cells
    Frederic Geissmann
    UPRES EA 219 Service d Anatomie Pathologique EA 219, Hopital Necker Enfants Malades, 161 rue de Sevres, 75743 Paris Cedex 15, France
    J Exp Med 198:623-34. 2003
    ..We identify a novel cellular function for retinoids and suggest that selective retinoids might be of interest for controlling antigen presentation...
  31. ncbi request reprint Clinical, immunologic and genetic analysis of 29 patients with autosomal recessive hyper-IgM syndrome due to Activation-Induced Cytidine Deaminase deficiency
    Pierre Quartier
    Hopital Necker Enfants Malades, Unité d immunologie hématologie et rhumatologie pédiatrique, Paris, France
    Clin Immunol 110:22-9. 2004
    ..In conclusion, AID-deficient patients are prone to infections and lymphoid hyperplasia, which may be prevented by early-onset IVIG replacement, but also to autoimmune and inflammatory disorders...
  32. ncbi request reprint The mechanisms of immune diversification and their disorders
    Jean Pierre de Villartay
    Dévelopement Normal et Pathologique du Système Immunitaire INSERM U429, Hopital Necker Enfants Malades, 149 rue de Sevres, 75015 Paris, France
    Nat Rev Immunol 3:962-72. 2003
  33. ncbi request reprint Human uracil-DNA glycosylase deficiency associated with profoundly impaired immunoglobulin class-switch recombination
    Kohsuke Imai
    Institut National de la Santé et de la Recherche Médicale Unité 429, Hopital Necker Enfants Malades, 75015 Paris, France
    Nat Immunol 4:1023-8. 2003
    ....
  34. doi request reprint Restoration of human B-cell differentiation into NOD-SCID mice engrafted with gene-corrected CD34+ cells isolated from Artemis or RAG1-deficient patients
    Chantal Lagresle-Peyrou
    Institut National de la Sante et de Recherche Medicale, Unit 768, Necker site, Paris, France
    Mol Ther 16:396-403. 2008
    ..This overall approach represents a useful tool for evaluating gene transfer efficiency in human SCID forms affecting B-cell development (such as Artemis deficiency) and for testing new vectors for improving in vivo RAG1 complementation...
  35. doi request reprint Hyper-immunoglobulin M syndrome type 3 with normal CD40 cell surface expression
    N E Karaca
    Ege University, The Medical School, Dept of Pediatrics, Division of Pediatric Immunology, Izmir, Turkey
    Scand J Immunol 76:21-5. 2012
    ..This observation emphasizes the requirement of CD40 mutation analysis for definite diagnosis of HIGM3 despite normal flow cytometric expression of CD40, particularly if the immunological and clinical profile is suggestive for HIGM3...
  36. ncbi request reprint Treatment of B-lymphoproliferative disorder with a monoclonal anti-interleukin-6 antibody in 12 patients: a multicenter phase 1-2 clinical trial
    E Haddad
    Unité d Immunologie et d Hématologie Pédiatriques, Service de Réanimation Pédiatrique and INSERM U429, Hopital Necker Enfants Malades, Paris, France
    Blood 97:1590-7. 2001
    ..These data suggest that the anti-IL-6 antibody is safe and should be further explored in the treatment of BLPD...
  37. pmc Human PMS2 deficiency is associated with impaired immunoglobulin class switch recombination
    Sophie Peron
    Institut National de Santé et de Recherche Médicale, U768, 75015 Paris, France
    J Exp Med 205:2465-72. 2008
    ..It is characterized by the defective occurrence of double-strand DNA breaks (DSBs) in switch regions and abnormal formation of switch junctions. This observation strongly suggests a role for PMS2 in CSR-induced DSB generation...
  38. ncbi request reprint Pathophysiology of B-cell intrinsic immunoglobulin class switch recombination deficiencies
    Anne Durandy
    INSERM, U768, Paris F 75015, France
    Adv Immunol 94:275-306. 2007
    ..Ig-CSR deficiencies 3 and 4 are characterized by a selective CSR defect resulting from blocks at distinct steps of CSR. A further understanding of the CSR machinery is expected from their molecular definition...
  39. pmc Efficacy of gene therapy for X-linked severe combined immunodeficiency
    Salima Hacein-Bey-Abina
    Department of Biotherapy, Necker Enfants Malades Hospital, Paris, France
    N Engl J Med 363:355-64. 2010
    ..We reviewed long-term outcomes after gene therapy in nine patients with X-linked severe combined immunodeficiency (SCID-X1), which is characterized by the absence of the cytokine receptor common gamma chain...
  40. pmc Function of Apollo (SNM1B) at telomere highlighted by a splice variant identified in a patient with Hoyeraal-Hreidarsson syndrome
    Fabien Touzot
    Institut National de la Sante et de la Recherche Medicale, U768, 75015 Paris, France
    Proc Natl Acad Sci U S A 107:10097-102. 2010
    ..These results identify Apollo as a crucial actor in telomere maintenance in vivo, independent of its function as a general DNA repair factor...
  41. pmc Immunoglobulin class switch recombination: study through human natural mutants
    Anne Durandy
    INSERM, U768, Paris 75015, France
    Philos Trans R Soc Lond B Biol Sci 364:577-82. 2009
    ..However, most of these CSR deficiencies remain molecularly undefined. Their characterization would lead to a better understanding of the complex machinery involved in CSR...
  42. ncbi request reprint Impairment of mycobacterial immunity in human interleukin-12 receptor deficiency
    F Altare
    INSERM U429, Hopital Necker Enfants Malades, Paris 75015, France
    Science 280:1432-5. 1998
    ..Thus, IL-12-dependent IFN-gamma secretion in humans seems essential in the control of mycobacterial infections, despite the formation of mature granulomas due to IL-12-independent IFN-gamma secretion...
  43. pmc Severe combined immunodeficiency caused by deficiency in either the delta or the epsilon subunit of CD3
    Genevieve De Saint Basile
    Unité Développement Normal et Pathologique du Système Immunitaire, INSERM U 429, Paris, France
    J Clin Invest 114:1512-7. 2004
    ..e., CD3epsilon deficiency, and emphasize the essential roles played by the CD3epsilon and CD3delta subunits in human thymocyte development, since these subunits associate with both the pre-TCR and the TCR...
  44. ncbi request reprint Ataxia-telangiectasia in twins presenting as autosomal recessive hyper-immunoglobulin M syndrome
    Amos Etzioni
    Department of Pediatrics, Meyer Children s Hospital, Haifa, Israel
    Isr Med Assoc J 9:406-7. 2007
  45. ncbi request reprint Molecular genetic analysis of Hungarian patients with the hyper-immunoglobulin M syndrome
    Melinda Erdos
    Department of Infectious and Pediatric Immunology, Medical and Health Science Center, University of Debrecen, Nagyerdei krt 98, H 4032 Debrecen, Hungary
    Mol Immunol 45:278-82. 2008
    ..This is the first comprehensive overview of molecular genetic features of Hungarian patients with HIGM syndrome...
  46. ncbi request reprint AID mutant analyses indicate requirement for class-switch-specific cofactors
    Van Thanh Ta
    Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida, Sakyo ku, Kyoto, 606 8501, Japan
    Nat Immunol 4:843-8. 2003
    ..These results indicate that AID requires interaction with a cofactor(s) specific to CSR...
  47. pmc Characterization of Ig gene somatic hypermutation in the absence of activation-induced cytidine deaminase
    Nancy S Longo
    Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892, USA
    J Immunol 181:1299-306. 2008
    ..Similar results were observed in V(L) rearrangements. The residual mutations were predominantly G:C substitutions, indicating that AICDA-independent cytidine deamination was a likely, yet inefficient, mechanism for mutating Ig genes...
  48. pmc Repair of U/G and U/A in DNA by UNG2-associated repair complexes takes place predominantly by short-patch repair both in proliferating and growth-arrested cells
    Mansour Akbari
    Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, N 7489 Trondheim, Norway
    Nucleic Acids Res 32:5486-98. 2004
    ..In conclusion, UNG2 is present in preassembled complexes proficient in BER. Furthermore, UNG2 is the major enzyme initiating BER of deaminated cytosine (U/G), and possibly the sole enzyme initiating BER of misincorporated uracil (U/A)...
  49. pmc B cells from hyper-IgM patients carrying UNG mutations lack ability to remove uracil from ssDNA and have elevated genomic uracil
    Bodil Kavli
    Department of Cancer Research and Molecular Medicine, Faculty of Medicine, Norwegian University of Science and Technology, N 7489 Trondheim, Norway
    J Exp Med 201:2011-21. 2005
    ..Based on our findings and recent information in the literature, we present an integrated model for the initiating steps in CSR...
  50. ncbi request reprint Defined blocks in terminal plasma cell differentiation of common variable immunodeficiency patients
    Nadine Taubenheim
    Clinical Research Unit for Rheumatology, University Hospital of Freiburg, Freiburg, Germany
    J Immunol 175:5498-503. 2005
    ..B cells reaching only the first stage of plasma cell differentiation were further unable to undergo isotype switching and to up-regulate activation markers on B cells stimulated in vitro...
  51. ncbi request reprint Memory switched B cell percentage and not serum immunoglobulin concentration is associated with clinical complications in children and adults with specific antibody deficiency and common variable immunodeficiency
    Hana Alachkar
    Department of Immunology, Hope Hospital, Manchester, UK
    Clin Immunol 120:310-8. 2006
    ....
  52. ncbi request reprint Defects of class-switch recombination
    Luigi D Notarangelo
    Department of Pediatrics and Angelo Nocivelli Institute for Molecular Medicine, University of Brescia Spedali Civili, Italy
    J Allergy Clin Immunol 117:855-64. 2006
    ....
  53. ncbi request reprint Human ICOS deficiency abrogates the germinal center reaction and provides a monogenic model for common variable immunodeficiency
    Klaus Warnatz
    Division of Rheumatology and Clinical Immunology, University Hospital, Freiburg, Germany
    Blood 107:3045-52. 2006
    ..Human ICOS deficiency is indistinguishable from CVID and thus serves as a monogenic model for this complex syndrome...
  54. ncbi request reprint A novel form of non-X-linked hyperigm associated with growth and pubertal disturbances and with lymphoma development
    Viviana Moschese
    Department of Pediatrics, University of Rome Tor Vergata, Italy
    J Pediatr 148:404-6. 2006
    ..We report on two female patients affected by a novel syndrome associating HIGM, growth and pubertal disturbances, and severe lymphoid hyperplasia with eventual development into lymphomas, suggesting a DNA repair defect...
  55. ncbi request reprint [Two years after, activation-induced cytidine deaminase has not revealed all of its secrets]
    Nadia Catalan
    Med Sci (Paris) 19:139-41. 2003
  56. pmc X-linked susceptibility to mycobacteria is caused by mutations in NEMO impairing CD40-dependent IL-12 production
    Orchidée Filipe-Santos
    Laboratory of Human Genetics of Infectious Diseases, University of Paris René Descartes Institut National de la Santé et de la Recherche Médicale INSERM U 550, Necker Medical School, Paris, France
    J Exp Med 203:1745-59. 2006
    ..They also demonstrate the importance of the T cell- and CD40L-triggered, CD40-, and NEMO/NF-kappaB/c-Rel-mediated induction of IL-12 by monocyte-derived cells for protective immunity to mycobacteria in humans...
  57. ncbi request reprint ICOS deficiency is associated with a severe reduction of CXCR5+CD4 germinal center Th cells
    Lukas Bossaller
    Division of Rheumatology and Clinical Immunology, University Clinic Freiburg, Hugstetterstrasse 55, D 79106 Freiburg, Germany
    J Immunol 177:4927-32. 2006
    ....