CD244 Molecule, Natural Killer Cell Receptor 2B4 (CD244) ELISA Kits

Human CD244 Molecule, Natural Killer Cell Receptor 2B4 (CD244) interaction partners

1. The Emerging Role of CD244 Signaling in Immune Cells of the Tumor Microenvironment.

2. Sole engagement of NKG2D, 2B4 or DNAM-1 is insufficient for NF-kappaB activation.

3. We determined a significantly lower expression of CD244 on monocytes in systemic lupus erythematosus patients compared to healthy controls. Furthermore, monocyte CD244 expression was negatively associated with several serum autoantibody titres.

4. SLAMF4 is a marker of intestinal immune cells which contributes to the protection against enteric pathogens and whose expression is dependent on the presence of the gut microbiota

5. The present study provides further insights into the role of the 2B4-CD48 interaction in the fine regulation of CD8(+) T-cell effector function upon antigenic stimulation.

6. Data show that 2B4 not only can bind to CD48 in trans but also interacts with CD48 in cis by using the same binding interface. Also, the results demonstrated that constitutive phosphorylation of 2B4 occurs only in the presence of CD48, and that cis binding is sufficient to induce substantial levels of baseline phosphorylation.

7. 2B4 expression is increased on CD4+ T cells in septic patients

8. Self-iNKR(-) NK cells in X-linked lymphoproliferative disease 1 patients are functional even in resting conditions, suggesting a role of the inhibitory 2B4/CD48 pathway in the education process during NK-cell maturation.

9. our results provide strong evidence that CD244 co-operates with c-Kit to regulate leukemogenesis through SHP-2/p27 signaling.

10. SLAMF4 gene and surface protein expression was down-regulated in CD8+ T cells from SLE patients compared with that in cells obtained from healthy donors. SLAMF4+ effector memory cells produced more granzyme B and perforin than SLAMF4- cells.

11. GSK-3 undergoes inhibitory phosphorylation at regulatory serine residues by the engagement of NKG2D and 2B4, either individually or in combination.

12. Cytomegalovirus-Induced Expression of CD244 after Liver Transplantation Is Associated with CD8+ T Cell Hyporesponsiveness to Alloantigen

13. CD8(+) T cells require 2B4 for Epstein-Barr virus-specific immune control, because 2B4 blockade after CD8(+) T-cell depletion did not further aggravate symptoms of the infection.

14. CD244 expression/signaling in tuberculosis correlates with high levels of a long noncoding RNA (lncRNA)-BC050410 [named as lncRNA-AS-GSTT1(1-72) or lncRNA-CD244] in the CD244(+)CD8(+) T-cell subpopulation.

15. show that in addition to NKG2D, human CEACAM1 can inhibit NK-cell activation via NKp30 or 2B4

16. this study investigates the structural requirements for the recruitment of the human-activating NK-cell receptors NKG2D and 2B4 to detergent-resistant membrane fractions in the murine BA/F3 cell line and in the human NK-cell line NKL.

17. Study of SAP expression is specific but may have insufficient sensitivity for screening XLP1 as a single tool; however, combination with 2B4 functional assay allows identification of all cases

18. Blockade of 2B4/CD48 interaction resulted in improvement in function via perforin expression and degranulation as measured by CD107a surface mobilization on HTLV-1 specific CD8+ T cells.

19. In patients suffering from X-linked lymphoproliferative disease (XLP1), SAP is nonfunctional, not only abolishing the activating function of 2B4, but rendering this receptor inhibitory.

20. XLP1 inhibitory effect by 2B4 does not affect DNAM-1 and NKG2D activating pathways in NK cells.

Mouse (Murine) CD244 Molecule, Natural Killer Cell Receptor 2B4 (CD244) interaction partners

1. Phenotypic analysis revealed an increased frequency of murine EBV homolog-specific CD8(+) T cells expressing the 2B4 coinhibitory receptor in septic animals compared with sham controls.

2. these data indicate that 2B4 signals function to alter T cell glucose metabolism, thereby limiting the proliferation and accumulation of CD8(+) T cells.

3. SLAMF4 is a marker of intestinal immune cells which contributes to the protection against enteric pathogens and whose expression is dependent on the presence of the gut microbiota

4. 2B4 expression is increased on CD4+ T cells in septic animals

5. 2B4 dampens T-independent B cell responses.

6. DCs from CD244(-/-) mice elicited increased NK cell activation in vitro. These data add CD244 to a growing list of immuno-modulatory receptors found on DCs.

7. Data show that enforced expression of inhibitor of differentiation protein Id3 specifically increased the persistence of Cd244 protein 2B4(+) virus-specific CD8(+) T cells.

8. Molecular dynamic simulation explains unbinding and unfolding of CD48-2B4 protein complexes.

9. Signaling via SLAMF4 controls expansion of cytotoxic CD8alphabeta(+) IELs, which regulate the reversible depletion of lamina propria phagocytes and inflammation in the small intestine.

10. CD244 (2B4) has a regulatory effect on mast cells and eosinophils in murine allergic inflammation.

11. NKG2D ligation relieves 2B4-mediated NK-cell self-tolerance in mice.

12. blockade of CD28 signals in the presence of preserved CTLA-4 signals results in the unique up-regulation of 2B4 on primary CD8(+) effectors, and that this 2B4 expression plays a critical functional role in controlling antigen-specific T8 cell responses

13. In the absence of SAP, signaling through the SLAM family members Ly108 and 2B4 resulted in increased recruitment of the SHP-1 phosphatase, associated with altered SHP-1 localization and decreased activation of Src kinases at the synapse.

14. Ox-LDL significantly promoted the interaction of natural killer cells and dendritic cells via CD48-2B4 contact-dependent mechanisms.

15. Slamf4 has a natural killer (NK) cell-independent negative regulatory function in vivo and can contribute to tolerance to chromatin in murine models of systemic lupus erythematosus.

16. CD48 on surrounding NK or non-NK cells serves primarily as a ligand to stimulate 2B4 on the adjacent NK cells in mice

17. The interaction of SHIP, 2B4 activating receptor, and the major histocompatibility complex influence the regulation of natural killer (NK) cell receptor repertoire, cytolytic function, and interferon-gamma production.

18. Regulation of CD8(+) T cell proliferation

19. Increased blood flow observed in response to topical application of capsaicin involves activation of NK 1 receptors.

20. Due to a CxC cysteine motif found in the transmembrane region, 2B4 localizes in glycolipid-enriched microdomains of NK and T cell plasma membranes, where it associates with LAT.