CS1 (CRACC, CD319) Induces Proliferation and Autocrine Cytokine Expression on Human B Lymphocytes1

No abstract is available for this paper.

• Publication year

  2007

• Venue

  Journal of Immunology

• Publication date

  2007-10-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.4049/jimmunol.179.7.4672PMID 17878365
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Immune regulation by SLAM family receptors and SAP-related adaptors

  2006cited by this paper
• Identification and characterization of two related murine genes, Eat2a and Eat2b, encoding single SH2-domain adapters

  2006cited by this paper
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  2005cited by this paper
• Molecular and functional characterization of a CS1 (CRACC) splice variant expressed in human NK cells that does not contain immunoreceptor tyrosine‐based switch motifs

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• Complementary Signaling through flt3 and Interleukin-7 Receptor α Is Indispensable for Fetal and Adult B Cell Genesis

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  2002cited by this paper
• Faculty Opinions recommendation of Activation of NK cell-mediated cytotoxicity by a SAP-independent receptor of the CD2 family.

  2002cited by this paper
• CS1, a novel member of the CD2 family, is homophilic and regulates NK cell function.

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  2001cited by this paper
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• The X-linked lymphoproliferative-disease gene product SAP regulates signals induced through the co-receptor SLAM

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• Soluble and Membrane-bound Forms of Signaling Lymphocytic Activation Molecule (SLAM) Induce Proliferation and Ig Synthesis by Activated Human B Lymphocytes

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• Tumor necrosis factor a is an autocrine growth factor for normal human B cells

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• Bruton's tyrosine kinase inhibitors rescue neuronal impairment caused by B cell-mediated lymphotoxin-α release.

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• Emerging roles of SLAMF7 in immune cells and related diseases

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• SLAMF7 (CD319) enhances cytotoxic T-cell differentiation and sensitizes CD8+ T cells to immune checkpoint blockade

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