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10.1016/j.jaci.2013.10.051

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suck abstract from ncbi


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pmid24373350
      J+Allergy+Clin+Immunol 2014 ; 133 (4 ): 1149-61
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  • Signaling lymphocytic activation molecule (SLAM)/SLAM-associated protein pathway regulates human B-cell tolerance #MMPMID24373350
  • Menard L ; Cantaert T ; Chamberlain N ; Tangye SG ; Riminton S ; Church JA ; Klion A ; Cunningham-Rundles C ; Nichols KE ; Meffre E
  • J Allergy Clin Immunol 2014[Apr]; 133 (4 ): 1149-61 PMID24373350 show ga
  • BACKGROUND: Signaling lymphocytic activation molecule (SLAM)-associated protein (SAP) can mediate the function of SLAM molecules, which have been proposed to be involved in the development of autoimmunity in mice. OBJECTIVE: We sought to determine whether the SLAM/SAP pathway regulates the establishment of human B-cell tolerance and what mechanisms of B-cell tolerance could be affected by SAP deficiency. METHODS: We tested the reactivity of antibodies isolated from single B cells from SAP-deficient patients with X-linked lymphoproliferative disease (XLP). The expressions of SAP and SLAM family members were assessed in human bone marrow-developing B cells. We also analyzed regulatory T (Treg) cell function in patients with XLP and healthy control subjects. RESULTS: We found that new emigrant/transitional B cells from patients with XLP were enriched in autoreactive clones, revealing a defective central B-cell tolerance checkpoint in the absence of functional SAP. In agreement with a B cell-intrinsic regulation of central tolerance, we identified SAP expression in a discrete subset of bone marrow immature B cells. SAP colocalized with SLAMF6 only in association with clustered B-cell receptors likely recognizing self-antigens, suggesting that SLAM/SAP regulate B-cell receptor-mediated central tolerance. In addition, patients with XLP displayed defective peripheral B-cell tolerance, which is normally controlled by Treg cells. Treg cells in patients with XLP seem functional, but SAP-deficient T cells were resistant to Treg cell-mediated suppression. Indeed, SAP-deficient T cells were hyperresponsive to T-cell receptor stimulation, which resulted in increased secretion of IL-2, IFN-?, and TNF-?. CONCLUSIONS: SAP expression is required for the counterselection of developing autoreactive B cells and prevents their T cell-dependent accumulation in the periphery.
  • |*Immune Tolerance [MESH]
  • |*Signal Transduction [MESH]
  • |Antigens, CD/*metabolism [MESH]
  • |Autoimmunity/genetics/immunology [MESH]
  • |B-Cell Activating Factor/blood [MESH]
  • |B-Lymphocytes/*immunology/*metabolism [MESH]
  • |Gene Expression [MESH]
  • |Humans [MESH]
  • |Intracellular Signaling Peptides and Proteins/deficiency/genetics/*metabolism [MESH]
  • |Lymphocyte Activation/immunology [MESH]
  • |Lymphoproliferative Disorders/genetics/immunology/metabolism [MESH]
  • |Protein Binding [MESH]
  • |Protein Transport [MESH]
  • |Receptors, Antigen, B-Cell/metabolism [MESH]
  • |Receptors, Cell Surface/*metabolism [MESH]
  • |Signaling Lymphocytic Activation Molecule Associated Protein [MESH]
  • |Signaling Lymphocytic Activation Molecule Family [MESH]
  • |Signaling Lymphocytic Activation Molecule Family Member 1 [MESH]


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