The gene defective in X-linked lymphoproliferative disease controls T cell dependent immune surveillance against Epstein–Barr virus
Our understanding of the X-linked lymphoproliferative syndrome (XLP) has advanced significantly in the past two years. The gene that is aberrant in the condition – SH2D1A/ SAP, which encodes SAP (signaling lymphocytic activation molecule [SLAM]-associated protein) – was cloned, the crystal structure...
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| Published in: | Current Opinion in Immunology Vol. 12; no. 4; pp. 474 - 478 |
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| Main Authors: | , , , |
| Format: | Book Review Journal Article |
| Language: | English |
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01-08-2000
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| Abstract | Our understanding of the X-linked lymphoproliferative syndrome (XLP) has advanced significantly in the past two years. The gene that is aberrant in the condition –
SH2D1A/
SAP, which encodes SAP (signaling lymphocytic activation molecule [SLAM]-associated protein) – was cloned, the crystal structure of its product was solved and insights into the signaling mechanisms of this small SH2-domain-containing protein via the cell surface receptors SLAM and 2B4 have been provided.
SAP mutation, and not Epstein–Barr virus infection per se, may be critical for XLP. |
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| AbstractList | Our understanding of the X-linked lymphoproliferative syndrome (XLP) has advanced significantly in the past two years. The gene that is aberrant in the condition - SH2D1A/SAP, which encodes SAP (signaling lymphocytic activation molecule [SLAM]-associated protein) - was cloned, the crystal structure of its product was solved and insights into the signaling mechanisms of this small SH2-domain-containing protein via the cell surface receptors SLAM and 2B4 have been provided. SAP mutation, and not Epstein-Barr virus infection per se, may be critical for XLP. Our understanding of the X-linked lymphoproliferative syndrome (XLP) has advanced significantly in the past two years. The gene that is aberrant in the condition - SH2D1A/SAP, which encodes SAP (signaling lymphocytic activation molecule [SLAM]-associated protein) - was cloned, the crystal structure of its product was sloved and insights into the signaling mechanisms of this small SH2-domain-containing protein via the cell surface receptors SLAM and 2B4 have been provided. SAP mutation, and not Epstein-Barr virus infection per se, may be critical for XLP. Our understanding of the X-linked lymphoproliferative syndrome (XLP) has advanced significantly in the past two years. The gene that is aberrant in the condition – SH2D1A/ SAP, which encodes SAP (signaling lymphocytic activation molecule [SLAM]-associated protein) – was cloned, the crystal structure of its product was solved and insights into the signaling mechanisms of this small SH2-domain-containing protein via the cell surface receptors SLAM and 2B4 have been provided. SAP mutation, and not Epstein–Barr virus infection per se, may be critical for XLP. |
| Author | Morra, Massimo Terhorst, Cox Howie, Duncan Sayos, Juan |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/10899030$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Antigens, CD Binding motif Carrier Proteins - genetics Carrier Proteins - immunology Cloning, Molecular Crystal structure Epstein-Barr virus Gene Deletion Glycoproteins - immunology Herpesvirus 4, Human - immunology Human Humans Immunoglobulins - immunology Intracellular Signaling Peptides and Proteins Lymphoproliferative Lymphoproliferative Disorders - genetics Lymphoproliferative Disorders - immunology Lymphoproliferative Disorders - virology Receptors, Antigen, T-Cell - immunology Receptors, Cell Surface SAP SAP gene SH2 SH21A/SAP gene SHD1A Signaling Lymphocytic Activation Molecule Associated Protein Signaling Lymphocytic Activation Molecule Family Member 1 SLAM T-Lymphocytes - immunology X-linked lymphoproliferative disease X-linked lymphoproliferative syndrome XLP |
| Title | The gene defective in X-linked lymphoproliferative disease controls T cell dependent immune surveillance against Epstein–Barr virus |
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