XIAP, un gène anti-apoptotique muté dans un nouveau syndrome lymphoprolifératif lié à l’X (XLP)

Stéphanie Rigaud; Sylvain Latour

doi:10.1051/medsci/2007233235

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Volume 23 / Numéro 3 (Mars 2007)

Med Sci (Paris), 23 3 (2007) 235-237

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Numéro		Med Sci (Paris) Volume 23, Numéro 3, Mars 2007


Page(s)		235 - 237
Section		Nouvelles
DOI		https://doi.org/10.1051/medsci/2007233235
Publié en ligne		15 mars 2007

Nichols KE, Ma CS, Cannons JL, et al. Molecular and cellular pathogenesis of X-linked lymphoproliferative disease. Immunol Rev 2005; 203 : 180–99. [Google Scholar]
De Saint Basile G, Fischer A. Defective cytotoxic granule-mediated cell death pathway impairs T lymphocyte homeostasis. Curr Opin Rheumatol 2003; 15 : 436–45. [Google Scholar]
Latour S, Gish G, Helgason CD, et al. Regulation of SLAM-mediated signal transduction by SAP, the X-linked lymphoproliferative gene product. Nat Immunol 2001; 2 : 681–90. [Google Scholar]
Rigaud S, Fondaneche MC, Lambert N, et al. XIAP deficiency in humans causes an X-linked lymphoproliferative syndrome. Nature 2006; 444 : 110–4. [Google Scholar]
Dupre L, Andolfi G, Tangye SG, et al. SAP controls the cytolytic activity of CD8⁺ T cells against EBV-infected cells. Blood 2005; 105 : 4383–9. [Google Scholar]
Parolini S, Bottino C, Falco M, et al. X-linked lymphoproliferative disease. 2B4 molecules displaying inhibitory rather than activating function are responsible for the inability of natural killer cells to kill Epstein-Barr virus-infected cells. J Exp Med 2000; 192 : 337–46. [Google Scholar]
Bottino C, Falco M, Parolini S, et al. NTB-A (correction of GNTB-A), a novel SH2D1A-associated surface molecule contributing to the inability of natural killer cells to kill Epstein-Barr virus-infected B cells in X-linked lymphoproliferative disease. J Exp Med 2001; 194 : 235–46. [Google Scholar]
Pasquier B, Yin L, Fondaneche MC, et al. Defective NKT cell development in mice and humans lacking the adapter SAP, the X-linked lymphoproliferative syndrome gene product. J Exp Med 2005; 201 : 695–701. [Google Scholar]
Nichols KE, Hom J, Gong SY, et al. Regulation of NKT cell development by SAP, the protein defective in XLP. Nat Med 2005; 11 : 340–5. [Google Scholar]
Salvesen GS, Duckett CS. IAP proteins: blocking the road to death’s door. Nat Rev Mol Cell Biol 2002; 3 : 401–10. [Google Scholar]
Rieux-Laucat F. Autoimmune lymphoproliferative syndrome: an inherited or a somatic defect of apoptosis. Med Sci (Paris) 2006; 22 : 645–9. [Google Scholar]
Lin Y, Roberts TJ, Wang CR, et al. Long-term loss of canonical NKT cells following an acute virus infection. Eur J Immunol 2005; 35 : 879–89. [Google Scholar]

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[1] Nichols KE, Ma CS, Cannons JL, et al. Molecular and cellular pathogenesis of X-linked lymphoproliferative disease. Immunol Rev 2005; 203 : 180–99. [Google Scholar]

[2] De Saint Basile G, Fischer A. Defective cytotoxic granule-mediated cell death pathway impairs T lymphocyte homeostasis. Curr Opin Rheumatol 2003; 15 : 436–45. [Google Scholar]

[3] Latour S, Gish G, Helgason CD, et al. Regulation of SLAM-mediated signal transduction by SAP, the X-linked lymphoproliferative gene product. Nat Immunol 2001; 2 : 681–90. [Google Scholar]

[4] Rigaud S, Fondaneche MC, Lambert N, et al. XIAP deficiency in humans causes an X-linked lymphoproliferative syndrome. Nature 2006; 444 : 110–4. [Google Scholar]

[5] Dupre L, Andolfi G, Tangye SG, et al. SAP controls the cytolytic activity of CD8⁺ T cells against EBV-infected cells. Blood 2005; 105 : 4383–9. [Google Scholar]

[6] Parolini S, Bottino C, Falco M, et al. X-linked lymphoproliferative disease. 2B4 molecules displaying inhibitory rather than activating function are responsible for the inability of natural killer cells to kill Epstein-Barr virus-infected cells. J Exp Med 2000; 192 : 337–46. [Google Scholar]

[7] Bottino C, Falco M, Parolini S, et al. NTB-A (correction of GNTB-A), a novel SH2D1A-associated surface molecule contributing to the inability of natural killer cells to kill Epstein-Barr virus-infected B cells in X-linked lymphoproliferative disease. J Exp Med 2001; 194 : 235–46. [Google Scholar]

[8] Pasquier B, Yin L, Fondaneche MC, et al. Defective NKT cell development in mice and humans lacking the adapter SAP, the X-linked lymphoproliferative syndrome gene product. J Exp Med 2005; 201 : 695–701. [Google Scholar]

[9] Nichols KE, Hom J, Gong SY, et al. Regulation of NKT cell development by SAP, the protein defective in XLP. Nat Med 2005; 11 : 340–5. [Google Scholar]

[10] Salvesen GS, Duckett CS. IAP proteins: blocking the road to death’s door. Nat Rev Mol Cell Biol 2002; 3 : 401–10. [Google Scholar]

[11] Rieux-Laucat F. Autoimmune lymphoproliferative syndrome: an inherited or a somatic defect of apoptosis. Med Sci (Paris) 2006; 22 : 645–9. [Google Scholar]

[12] Lin Y, Roberts TJ, Wang CR, et al. Long-term loss of canonical NKT cells following an acute virus infection. Eur J Immunol 2005; 35 : 879–89. [Google Scholar]