Killer Cell Lectin-Like Receptor Subfamily C, Member 1 (KLRC1) Kits ELISA

Human Killer Cell Lectin-Like Receptor Subfamily C, Member 1 (KLRC1) interaction partners

1. NKp46(neg-low)/CD56(dim)/CD16(neg) cells displayed a markedly defective cytotoxicity that could be reversed by blocking the inhibitory receptor CD94/NKG2A. These data open new and important perspectives to better understand the ontogenesis/homeostasis of human natural killer cells and to develop a novel immune-therapeutic approach that targets the inhibitory NKG2A check-point.

2. Increased HLA-E expression contributes to persistence of senescent cells in tissues via interaction with the inhibitory receptor NKG2A expressed by NK and highly differentiated CD8(+) T cells to inhibit immune responses against senescent cells.

3. Compared with NKG2D, NKG2A expressed on both peripheral CD3-CD56+NK cells and CD3+CD8+T cells plays a more pivotal negative regulatory role in the progression of HBV-related ACLF.

4. These results indicate NKG2A inhibitory receptor may play a key role in transfusion-induced immunodepression of NK cells in patients with b-thalassemia major

5. Collectively, these results provide evidence for the first time that CD94/NKG2C is involved in chronic graft-versus-host disease prevention

6. CD94 and NKG2A polymorphisms may contribute to genetic susceptibility to rheumatoid arthritis or affect the response to anti-TNF therapy in patients of Caucasian origin.

7. NK cell maturation to CD56(dim) subset associated with high levels of NCRs overrides the inhibitory effect of NKG2A and recovers impaired NK cell cytolytic potential after allogeneic hematopoietic stem cell transplantation.

8. Coengagement of inhibitory receptors, either KIR2DL1 or CD94-NKG2A, did not inhibit phosphorylation of Stat5 but inhibited selectively phosphorylation of Akt and S6 ribosomal protein.

9. The presence of TIM3+and/or NKG2A+ T cells is associated with the absence of recurrences and a longer recurrence-free survival.

10. Balance between activating NKG2D, DNAM-1, NKp44 and NKp46 and inhibitory CD94/NKG2A receptors determine natural killer degranulation towards rheumatoid arthritis synovial fibroblasts.

11. Results suggested that the low expression level of CD94/NKG2A upon gammadelta T cell activation might lead to the over-activation of gammadelta T cells in patients with SLE.

12. The positive expression rate of NKG2D and NKG2A on NK cells and CD3(+) T cells in ALL patients was no significantly different from that in AML patients.

13. The level of NKG2A expression on resting CD8-positive T cells inversely correlated with acquisition of regulatory function when activated.

14. These results suggested that these glycans can interact with NKG2D and CD94 to modulate NK cell-dependent cytotoxicity.

15. The differences of CD94 and NKG2 expression between nasal NK/T-cell lymphomas and B cell lymphoma or T cell lymphoma were statistically significant.

16. NKG2A expression on gammadelta lymphoproliferative Disease of Large Granular Lymphocytes correlates with asymptomatic pathology, even in the presence of NKG2C coexpression.

17. CD56(dim) NK cells continue to differentiate. During this process, they lose expression of NKG2A, sequentially acquire inhibitory killer cell inhibitory immunoglobulin-like receptors and CD57.

18. a new model in which the NK cell differentiation and functional fate are based on a stepwise decrease of NKG2A and acquisition of KIRs

19. NK cell NKG2A expression is dysregulated in chronic hepatitis C. NKG2A-positive NK cells are associated with a beneficial response to pegylated interferon and ribavirin therapy.

20. Results sugges that KLRC1 can be a probable candidate gene for SLE on 12p12.3-13.2, but which is not associated with the disease activity.

Mouse (Murine) Killer Cell Lectin-Like Receptor Subfamily C, Member 1 (KLRC1) interaction partners

1. Data suggest that the Cd94(LocA)/NKG2A receptor (NKG2A) heterodimeric receptor is widely expressed among M. musculus subspecies musculus.

2. Liver cNK cells' hyporesponsiveness to stimulation through activating receptors is independent of IL-10, but correlates with decreased NKG2A expression compared to trNK cells.

3. Here, we provide a new anti-inflammation mechanism about ANXA1 secreted from injured IECs, where ANXA1 can stimulate the expression of NKG2A in NK cells that affect the recruitment and activity of neutrophils necessary for pathology of colitis.

4. NKG2A optimizes CD8(+) T cell responses during an acute poxvirus infection.

5. Results demonstrate the immunoregulatory role of CD8(+) NKG2A expression in virus infection, which negatively regulates T cell effector functions and contributes to protection of tissue integrity during virus clearance.

6. role in NK cell-mediated protection from DSS-induced colitis

7. Endogenous NKG2A contributes to the rejection of cells lacking human HLA-Cw3.

8. The complex interplay between various stimuli may account for the variable expression of CD94/NKG2A during responses to different pathogens in vivo.

9. expression of CD94 and its associated NKG2A, NKG2C, and NKG2E subunits is dispensable for NK cell development, education, and many NK cell functions

10. The NKG2A+KLRG1+ positive phenotype correlates with protective efficacy during antigenic recall from a pool of CD8 T cells during persistent gamma-herpesvirus 68 infection.

11. Data suggest that the liver environment regulates NK cell receptor expression and that IL-10 contributes to the regulation of liver NK cells, in part, by maintaining a greater percentage of the hyporesponsive NKG2A(+)Ly49(-) NK cells in the liver.

12. Implications of CD94 deficiency and monoallelic NKG2A expression for natural killer cell development and repertoire formation.

13. the CD94/NKG2A inhibitory receptor plays a critical role in down-regulating invariant NK-cell responses

14. results indicate that LTbetaR-mediated signals are not required for Ly49 and CD94/NKG2 receptor acquisition on NK cells

15. An NKG2B isoform paired with a CD94 alternatively spliced transcript may contribute to the plasticity of the natural killer cell immunological synapse by insuring an adequate inhibitory signal.

16. NKG2A-expressing anti-polyoma virus CD8 T cells appear to be essential for antigen-specific recall responses in mice persistently infected by polyoma virus.

17. Qa-1-NKG2A interaction protected activated CD4+ T cells from lysis by a subset of NKG2A+ natural-killer cells

18. CD94/NKG2A transduces a biologically important signal in vivo to activated CD8+ T cells that limits immunopathology in severe influenza infection.

19. genetic disruption of the Qa-1-CD94/NKG2A interaction unleashes robust CD8 Treg cell activity that completely abolishes development of experimental allergic encephalomyelitis