2B4 (CD244) and CS1: novel members of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes

@article{Boles20012B4A,
  title={2B4 (CD244) and CS1: novel members of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer cells and other leukocytes},
  author={Kent S. Boles and Susan E. Stepp and Michael J. Bennett and Vinay Kumar and Porunelloor A Mathew},
  journal={Immunological Reviews},
  year={2001},
  volume={181}
}
Summary: 2B4 is a member of the CD2 subset of the immunoglobulin superfamily molecules expressed on natural killer (NK) cells and other leukocytes. It is the high affinity ligand for CD48. Engagement of 2B4 on NK‐cell surfaces with specific antibodies or CD48 can trigger cell‐mediated cytotoxicity, interferon‐γ secretion, phosphoinositol turnover and NK‐cell invasiveness. The function of 2B4 in CD8+ T cells and myeloid cells remains unknown. The cytoplasmic domain of 2B4 contains unique… 

Protein kinase C is involved in 2B4 (CD244)‐mediated cytotoxicity and AP‐1 activation in natural killer cells

TLDR
The present study indicated that PKC may play an important role in 2B4 signalling and activator protein‐1 activation and treatment with the PKC inhibitor resulted in inhibition of natural cytotoxicity and redirected antibody‐dependent cellular cytot toxicity.

The CD2 family of natural killer cell receptors.

TLDR
A novel mechanism for lymphocyte regulation has emerged: CD2 family members on NK cells engage ligands on neighboring NK cells, leading to NK cell stimulation, which provides interlymphocyte communication that maintains organization within the hematopoietic compartment and amplifies immune responses.

Roles of NK Cell Receptors 2B4 (CD244), CS1 (CD319), and LLT1 (CLEC2D) in Cancer

TLDR
NK cell receptors 2B4, CS1, and LLT1 are described and their potential in targeting cancer cells for NK-cell-mediated immunotherapy is described and revealed thatLLT1 is expressed on prostate cancer and triple-negative breast cancer cells and allows them to evade NK- cell-mediated killing.

Molecular Basis of the Dual Functions of 2B4 (CD244)1

TLDR
The studies reveal that both human and mouse 2B4 can activate or inhibit NK cells, and demonstrate how a single receptor can have opposing function depending on the degree of receptor expression, extent of its ligation, and the relative abundance of certain adaptor molecules.

CD48: A co-stimulatory receptor of immunity.

A novel interface consisting of homologous immunoglobulin superfamily members with multiple functions

TLDR
The findings that CD155/poliovirus receptor (PVR) and CD112/nectin-2 are the ligands for CD226/platelet and T-cell activation antigen 1 (PTA1)/DNAX accessory molecular-1 (DNAM-1), CD96/tactile and Washington University cell adhesion molecule (WUCAM) have largely expanded knowledge about the functions of CD226, CD96, WUCAM and LFA-1.

Molecular basis for positive and negative signaling by the natural killer cell receptor 2B4 (CD244).

TLDR
The molecular basis for the different signals generated by 2B4 is investigated, showing that the first immunoreceptor tyrosine-based switch motif (ITSM) within the cytoplasmic tail of 2 B4 is sufficient for2B4-mediated NK-cell activation, whereas the third ITSM can negatively influence 2B 4 signaling.

The Adaptor Protein 3BP2 Binds Human CD244 and Links this Receptor to Vav Signaling, ERK Activation, and NK Cell Killing1

TLDR
Results indicate thatCD244-3BP2 association regulates cytolytic function but not IFN-γ release, reinforcing the hypothesis that, in humans, CD244-mediated cytotoxicity and IFN -γ release involve distinct NK pathways.

Mouse novel Ly9: a new member of the expanding CD150 (SLAM) family of leukocyte cell-surface receptors

TLDR
Mouse novel Ly9 is a new member of the expanding CD150 family of cell surface receptors, and it is shown that SAP (SH2D1A), an adapter protein responsible for the X-linked lymphoproliferative disease, binds to the phosphorylated cytoplasmic tail of human but not mouse novel Ly 9.
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