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CLEC9A is a group V C-type lectin-like receptor (CTLR) that functions as an activation receptor and is expressed on myeloid lineage cells (Huysamen et al., 2008 [PubMed 18408006]).[supplied by OMIM, Aug 2008].. Zusätzlich bieten wir Ihnen CLEC9A Antikörper (159) und CLEC9A Proteine (7) und viele weitere Produktgruppen zu diesem Protein an.
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Clec9a is responsible for the antigen cross-presentation of dendritic cell subsets and may be a target of immunotherapy
findings demonstrate that CLEC9A is a specialized receptor that modulates the innate immune response when there is a mycobacterial infection
Data indicate that blood dendritic cell antigen 3 BDCA3 (zeige THBD ELISA Kits)(+) and C-type lectin (zeige MBL2 ELISA Kits) domain family 9, member A (zeige CXCL14 ELISA Kits) CLEC9A(+) dendritic cells (DC) are of major importance in the induction of anti-viral and anti-tumor immunity.
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.
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
High expression of DNGR-1 specifically and universally identifies a unique dendritic cells subset in mouse and humans.
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.
Data show that CLEC9A is only expressed on immature BDCA3 (zeige THBD ELISA Kits)(+) myeloid dendritic cells (mDCs).
For production of cytotoxic T cells, transge (zeige LY75 ELISA Kits)nic DEC-205 and Clec9A, but (zeige CLEC12A ELISA Kits)not Clec12A, are effective targets for antibody-mediated delivery of antigens for vaccination, although only in the presence of adjuvants.
A population of human dendritic cells (DC) that expresses DNGR-1 (CLEC9A) and high levels of BDCA3 (zeige THBD ELISA Kits) and resembles mouse CD8alpha+ DCs in phenotype and function, is characterized.
Clec9A and Clec12A exhibit different intrinsic capacities to elicit MHC I and MHC II presentation following direct antigen targeting
DNGR-1 also regulated Trm cell generation.
A specific deletion of DNGR-1 limits the development of atherosclerosis and vascular inflammation.
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.
Study found presence of DNGR-1 in the brain, providing a potential marker for the study of a specific denditritic brain cell subset
A dependence on DNGR-1 for RSV-specific CD8 (zeige CD8A ELISA Kits)(+) T-cell responses was observed.
Genetic tracing of DNGR-1 expression history specifically marks cells traditionally ascribed to the dendritic cells lineage, and this restriction is maintained after inflammation.
Clec9A-positive dendritic cells control susceptibility of mice to experimental cerebral malaria.
Loss of DNGR-1 impaired the CD8 (zeige CD8A ELISA Kits) positive lymphocyte cytotoxic response to vaccinia virus, especially against those virus strains that are most dependent on cross-presentation.
CLEC9A is a group V C-type lectin-like receptor (CTLR) that functions as an activation receptor and is expressed on myeloid lineage cells (Huysamen et al., 2008
C-type lectin domain family 9 member A
, dendritic cell natural killer lectin group receptor 1