anti-C-Type Lectin Domain Family 9, Member A (CLEC9A) Antibodies

Mouse (Murine) C-Type Lectin Domain Family 9, Member A (CLEC9A) interaction partners

1. Myosin II-deficient necrotic cells are impaired in their ability to stimulate DNGR-1 or to serve as substrates for Conventional type 1 dendritic cells cross-presentation to CD8(+) T cells.

2. Self-adjuvanting nanoemulsion targeting dendritic cell receptor Clec9A enables antigen-specific immunotherapy.

3. DNGR-1 deficiency leads to exacerbated caerulein-induced necrotizing pancreatitis and increased pathology during systemic Candida albicans infection without affecting fungal burden.

4. Clec9A and Clec12A exhibit different intrinsic capacities to elicit MHC I and MHC II presentation following direct antigen targeting

5. DNGR-1 also regulated Trm cell generation.

6. A specific deletion of DNGR-1 limits the development of atherosclerosis and vascular inflammation.

7. The authors describe a conformational change that occurs in the neck region of DNGR-1 in a pH- and ionic strength-dependent manner and that controls cross-presentation of dead cell-associated antigens.

8. Study found presence of DNGR-1 in the brain, providing a potential marker for the study of a specific denditritic brain cell subset

9. A dependence on DNGR-1 for RSV-specific CD8(+) T-cell responses was observed.

10. Genetic tracing of DNGR-1 expression history specifically marks cells traditionally ascribed to the dendritic cells lineage, and this restriction is maintained after inflammation.

11. Clec9A-positive dendritic cells control susceptibility of mice to experimental cerebral malaria.

12. High expression of DNGR-1 specifically and universally identifies a unique dendritic cells subset in mouse and humans.

13. Loss of DNGR-1 impaired the CD8 positive lymphocyte cytotoxic response to vaccinia virus, especially against those virus strains that are most dependent on cross-presentation.

14. DNGR-1 regulated cross-priming in non-infectious settings such as immunization with antigen-bearing dead cells, as well as in highly immunogenic situations such as infection with herpes simplex virus type 1.

15. propose that Clec9A provides targeted recruitment of the adaptive immune system during infection and can also be utilized to enhance immune responses generated by vaccines.

16. Data show that targeting of antigen to Clec9A in batf3 null mice produced enhanced antibody responses.

17. For production of cytotoxic T cells, DEC-205 and Clec9A, but not Clec12A, are effective targets for antibody-mediated delivery of antigens for vaccination, although only in the presence of adjuvants.

18. Comparable T helper 1 (Th1) and CD8 T-cell immunity by targeting HIV gag p24 to CD8 dendritic cells within antibodies to Langerin, DEC205, and Clec9A.

19. CLEC9A functions as an activation receptor

20. DC, NK lectin group receptor-1 (DNGR-1) is a C-type lectin of the NK cell receptor group

Human C-Type Lectin Domain Family 9, Member A (CLEC9A) interaction partners

1. Clec9a is responsible for the antigen cross-presentation of dendritic cell subsets and may be a target of immunotherapy

2. findings demonstrate that CLEC9A is a specialized receptor that modulates the innate immune response when there is a mycobacterial infection

3. Data indicate that blood dendritic cell antigen 3 BDCA3(+) and C-type lectin domain family 9, member A CLEC9A(+) dendritic cells (DC) are of major importance in the induction of anti-viral and anti-tumor immunity.

4. Activated dendritic cell subsets expressing CD141/CLEA9A/CD1c, likely recruited into the tubulointerstitium, are positioned to play a role in the development of fibrosis and, thus, progression to chronic kidney disease.

5. study showsn that the DNGR-1 ligand is preserved from yeast to man and corresponds to the F-actin component of the cellular cytoskeleton; identification of F-actin as a DNGR-1 ligand suggests that cytoskeletal exposure is a universal sign of cell damage that can be targeted by the innate immune system to initiate immunity

6. High expression of DNGR-1 specifically and universally identifies a unique dendritic cells subset in mouse and humans.

7. propose that Clec9A provides targeted recruitment of the adaptive immune system during infection and can also be utilized to enhance immune responses generated by vaccines.

8. Data show that CLEC9A is only expressed on immature BDCA3(+) myeloid dendritic cells (mDCs).

9. For production of cytotoxic T cells, transgenic DEC-205 and Clec9A, but not Clec12A, are effective targets for antibody-mediated delivery of antigens for vaccination, although only in the presence of adjuvants.

10. A population of human dendritic cells (DC) that expresses DNGR-1 (CLEC9A) and high levels of BDCA3 and resembles mouse CD8alpha+ DCs in phenotype and function, is characterized.

11. The paper cited (J Clin Invest. 2008 Jun;118(6):2098-110) is the first characterization of human and mouse CLEC9A (a.k.a DNGR-1)

12. CLEC9A functions as an activation receptor

13. analysis of differences between mouse and human Clec9A

14. CLEC9A functions as a SYK-coupled C-type lectin receptor to mediate sensing of necrosis by the principal dendritic-cell subset involved in regulating cross-priming to cell-associated antigens