-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
News on April 7, 2021 //--- Natalizumab is a humanized monoclonal antibody (mAb) directed against α4-integrin, which is currently being used clinically for treatment For multiple sclerosis (MS), the drug can effectively reduce the number of dendritic cells (DC) around the cerebral blood vessels.
In this regard, a possible hypothesis is that the absence of α4-integrin in CD11c + cells can reduce their migration to the central nervous system (CNS), thereby improving experimental autoimmune encephalomyelitis (EAE) .
In a study recently published in the journal PNAS, Olaf Stüve's group from the University of Texas Southwestern Medical Center verified this hypothesis.
In this regard, a possible hypothesis is that the absence of α4-integrin in CD11c + cells can reduce their migration to the central nervous system (CNS), thereby improving experimental autoimmune encephalomyelitis (EAE) .
In a study recently published in the journal PNAS, Olaf Stüve's group from the University of Texas Southwestern Medical Center verified this hypothesis.
(Image source:the authors constructed and bred a mutant mouse called CD11c Cre +/- ITGA4fl/fl, in which α4-integrin was selectively knocked out in dendritic cells.
After that, the author established a mouse meningitis model based on immunization and adoptive transfer technology.
After that, the author established a mouse meningitis model based on immunization and adoptive transfer technology.
On this basis, the authors analyzed the indications of CD11c+ dendritic cells in the mouse brain and peripheral lymphoid organs through flow cytometry and single-cell sequencing, and compared them with wild-type controls.
(Figure 1.
The expression level of α 4-integrin in dendritic cells in CD11c Cre +/- ITGA4fl/fl mice was significantly reduced )
The expression level of α 4-integrin in dendritic cells in CD11c Cre +/- ITGA4fl/fl mice was significantly reduced )
The authors found that in the primary and secondary lymphoid organs of CD11c Cre +/- ITGA4fl/fl mice, the expression level of α4-integrin in CD11c + dendritic cells was significantly reduced, thus verifying the gene knockout efficiency of the mouse .
Later, the authors found that during the EAE induction process, the onset time of CD11c.
Cre +/- ITGA4fl/fl mice was significantly longer than that of the wild-type control.
In addition, CD11c + CD88 + cells were isolated in the blood during this period.
After the occurrence of EAE, the authors found that a group of CD11c + CD88 + cells accumulated in the central nervous system area, and expressed CD317 with high expression.
In the EAE model induced by adoptive transfer, the authors found that the clinical disease phenotype of CD11c.
Cre +/- ITGA4fl/fl mice was significantly improved compared to the wild-type control.
In addition, the number of CD11c + CD88 + CD317 + cells in the central nervous system Significantly reduced.
Later, the authors found that during the EAE induction process, the onset time of CD11c.
Cre +/- ITGA4fl/fl mice was significantly longer than that of the wild-type control.
In addition, CD11c + CD88 + cells were isolated in the blood during this period.
After the occurrence of EAE, the authors found that a group of CD11c + CD88 + cells accumulated in the central nervous system area, and expressed CD317 with high expression.
In the EAE model induced by adoptive transfer, the authors found that the clinical disease phenotype of CD11c.
Cre +/- ITGA4fl/fl mice was significantly improved compared to the wild-type control.
In addition, the number of CD11c + CD88 + CD317 + cells in the central nervous system Significantly reduced.
(Figure 2, CD11c Cre +/- ITGA4fl/fl mouse EAE disease progression is significantly improved compared to wild type )
On this basis, the author compared this finding with clinical patient information.
The results showed that in the cerebrospinal fluid of patients with neuroinflammation, microglia-like cells showed high expression of ITGAX (CD11c), C5AR1 (CD88), and BST2 (CD317), which was in line with those observed in mouse models.
The phenomenon is very consistent.
In the mouse model, the authors found that only activated glial cells (not in their natural state) can express CD11c, CD88 and CD317.
The results showed that in the cerebrospinal fluid of patients with neuroinflammation, microglia-like cells showed high expression of ITGAX (CD11c), C5AR1 (CD88), and BST2 (CD317), which was in line with those observed in mouse models.
The phenomenon is very consistent.
In the mouse model, the authors found that only activated glial cells (not in their natural state) can express CD11c, CD88 and CD317.
Finally, the author administered anti-CD317 antibody treatment after the onset of EAE symptoms in mice, and the results showed that the therapy can greatly improve the recovery ability of mice.
In summary, the authors revealed the potential of targeting CD137 as a new therapy for clinical multiple sclerosis.
(Bioon.
com)
In summary, the authors revealed the potential of targeting CD137 as a new therapy for clinical multiple sclerosis.
(Bioon.
com)
Original source: Navid Manouchehri, Rehana Z.
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
On this basis, the authors analyzed the indications of CD11c+ dendritic cells in the mouse brain and peripheral lymphoid organs through flow cytometry and single-cell sequencing, and compared them with wild-type controls.
(Figure 1.
The expression level of α 4-integrin in dendritic cells in CD11c Cre +/- ITGA4fl/fl mice was significantly reduced )
The expression level of α 4-integrin in dendritic cells in CD11c Cre +/- ITGA4fl/fl mice was significantly reduced )
The authors found that in the primary and secondary lymphoid organs of CD11c Cre +/- ITGA4fl/fl mice, the expression level of α4-integrin in CD11c + dendritic cells was significantly reduced, thus verifying the gene knockout efficiency of the mouse .
Later, the authors found that during the EAE induction process, the onset time of CD11c.
Cre +/- ITGA4fl/fl mice was significantly longer than that of the wild-type control.
In addition, CD11c + CD88 + cells were isolated in the blood during this period.
After the occurrence of EAE, the authors found that a group of CD11c + CD88 + cells accumulated in the central nervous system area, and expressed CD317 with high expression.
In the EAE model induced by adoptive transfer, the authors found that the clinical disease phenotype of CD11c.
Cre +/- ITGA4fl/fl mice was significantly improved compared to the wild-type control.
In addition, the number of CD11c + CD88 + CD317 + cells in the central nervous system Significantly reduced.
Later, the authors found that during the EAE induction process, the onset time of CD11c.
Cre +/- ITGA4fl/fl mice was significantly longer than that of the wild-type control.
In addition, CD11c + CD88 + cells were isolated in the blood during this period.
After the occurrence of EAE, the authors found that a group of CD11c + CD88 + cells accumulated in the central nervous system area, and expressed CD317 with high expression.
In the EAE model induced by adoptive transfer, the authors found that the clinical disease phenotype of CD11c.
Cre +/- ITGA4fl/fl mice was significantly improved compared to the wild-type control.
In addition, the number of CD11c + CD88 + CD317 + cells in the central nervous system Significantly reduced.
(Figure 2, CD11c Cre +/- ITGA4fl/fl mouse EAE disease progression is significantly improved compared to wild type )
On this basis, the author compared this finding with clinical patient information.
The results showed that in the cerebrospinal fluid of patients with neuroinflammation, microglia-like cells showed high expression of ITGAX (CD11c), C5AR1 (CD88), and BST2 (CD317), which was in line with those observed in mouse models.
The phenomenon is very consistent.
In the mouse model, the authors found that only activated glial cells (not in their natural state) can express CD11c, CD88 and CD317.
The results showed that in the cerebrospinal fluid of patients with neuroinflammation, microglia-like cells showed high expression of ITGAX (CD11c), C5AR1 (CD88), and BST2 (CD317), which was in line with those observed in mouse models.
The phenomenon is very consistent.
In the mouse model, the authors found that only activated glial cells (not in their natural state) can express CD11c, CD88 and CD317.
Finally, the author administered anti-CD317 antibody treatment after the onset of EAE symptoms in mice, and the results showed that the therapy can greatly improve the recovery ability of mice.
In summary, the authors revealed the potential of targeting CD137 as a new therapy for clinical multiple sclerosis.
(Bioon.
com)
In summary, the authors revealed the potential of targeting CD137 as a new therapy for clinical multiple sclerosis.
(Bioon.
com)
Original source: Navid Manouchehri, Rehana Z.
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
(Figure 1.
The expression level of α 4-integrin in dendritic cells in CD11c Cre +/- ITGA4fl/fl mice was significantly reduced )
The expression level of α 4-integrin in dendritic cells in CD11c Cre +/- ITGA4fl/fl mice was significantly reduced ) The expression level of α 4-integrin in dendritic cells in CD11c Cre +/- ITGA4fl/fl mice was significantly reduced )
The authors found that in the primary and secondary lymphoid organs of CD11c Cre +/- ITGA4fl/fl mice, the expression level of α4-integrin in CD11c + dendritic cells was significantly reduced, thus verifying the gene knockout efficiency of the mouse .
Later, the authors found that during the EAE induction process, the onset time of CD11c.
Cre +/- ITGA4fl/fl mice was significantly longer than that of the wild-type control.
In addition, CD11c + CD88 + cells were isolated in the blood during this period.
After the occurrence of EAE, the authors found that a group of CD11c + CD88 + cells accumulated in the central nervous system area, and expressed CD317 with high expression.
In the EAE model induced by adoptive transfer, the authors found that the clinical disease phenotype of CD11c.
Cre +/- ITGA4fl/fl mice was significantly improved compared to the wild-type control.
In addition, the number of CD11c + CD88 + CD317 + cells in the central nervous system Significantly reduced.
Later, the authors found that during the EAE induction process, the onset time of CD11c.
Cre +/- ITGA4fl/fl mice was significantly longer than that of the wild-type control.
In addition, CD11c + CD88 + cells were isolated in the blood during this period.
After the occurrence of EAE, the authors found that a group of CD11c + CD88 + cells accumulated in the central nervous system area, and expressed CD317 with high expression.
In the EAE model induced by adoptive transfer, the authors found that the clinical disease phenotype of CD11c.
Cre +/- ITGA4fl/fl mice was significantly improved compared to the wild-type control.
In addition, the number of CD11c + CD88 + CD317 + cells in the central nervous system Significantly reduced.
(Figure 2, CD11c Cre +/- ITGA4fl/fl mouse EAE disease progression is significantly improved compared to wild type )
On this basis, the author compared this finding with clinical patient information.
The results showed that in the cerebrospinal fluid of patients with neuroinflammation, microglia-like cells showed high expression of ITGAX (CD11c), C5AR1 (CD88), and BST2 (CD317), which was in line with those observed in mouse models.
The phenomenon is very consistent.
In the mouse model, the authors found that only activated glial cells (not in their natural state) can express CD11c, CD88 and CD317.
The results showed that in the cerebrospinal fluid of patients with neuroinflammation, microglia-like cells showed high expression of ITGAX (CD11c), C5AR1 (CD88), and BST2 (CD317), which was in line with those observed in mouse models.
The phenomenon is very consistent.
In the mouse model, the authors found that only activated glial cells (not in their natural state) can express CD11c, CD88 and CD317.
Finally, the author administered anti-CD317 antibody treatment after the onset of EAE symptoms in mice, and the results showed that the therapy can greatly improve the recovery ability of mice.
In summary, the authors revealed the potential of targeting CD137 as a new therapy for clinical multiple sclerosis.
(Bioon.
com)
In summary, the authors revealed the potential of targeting CD137 as a new therapy for clinical multiple sclerosis.
(Bioon.
com)
Original source: Navid Manouchehri, Rehana Z.
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
(Figure 2, CD11c Cre +/- ITGA4fl/fl mouse EAE disease progression is significantly improved compared to wild type )
CD11c Cre +/- ITGA4fl/fl mouse EAE disease progression is significantly improved compared to wild type ) On this basis, the author compared this finding with clinical patient information.
The results showed that in the cerebrospinal fluid of patients with neuroinflammation, microglia-like cells showed high expression of ITGAX (CD11c), C5AR1 (CD88), and BST2 (CD317), which was in line with those observed in mouse models.
The phenomenon is very consistent.
In the mouse model, the authors found that only activated glial cells (not in their natural state) can express CD11c, CD88 and CD317.
The results showed that in the cerebrospinal fluid of patients with neuroinflammation, microglia-like cells showed high expression of ITGAX (CD11c), C5AR1 (CD88), and BST2 (CD317), which was in line with those observed in mouse models.
The phenomenon is very consistent.
In the mouse model, the authors found that only activated glial cells (not in their natural state) can express CD11c, CD88 and CD317.
Finally, the author administered anti-CD317 antibody treatment after the onset of EAE symptoms in mice, and the results showed that the therapy can greatly improve the recovery ability of mice.
In summary, the authors revealed the potential of targeting CD137 as a new therapy for clinical multiple sclerosis.
(Bioon.
com)
In summary, the authors revealed the potential of targeting CD137 as a new therapy for clinical multiple sclerosis.
(Bioon.
com)
Original source: Navid Manouchehri, Rehana Z.
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
Finally, the author administered anti-CD317 antibody treatment after the onset of EAE symptoms in mice, and the results showed that the therapy can greatly improve the recovery ability of mice.
In summary, the authors revealed the potential of targeting CD137 as a new therapy for clinical multiple sclerosis.
(Bioon.
com)
In summary, the authors revealed the potential of targeting CD137 as a new therapy for clinical multiple sclerosis.
(Bioon.
com)
Original source: Navid Manouchehri, Rehana Z.
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
Original source: Navid Manouchehri, Rehana Z.
Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
Original source: CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity. Hussain, Petra D.
Cravens et al.
, CD11c+CD88+CD317+ myeloid cells are critical mediators of persistent CNS autoimmunity.
Proceedings of the National Academy of Sciences Apr 2021, 118 (14) e2014492118; DOI: 10.
1073/pnas.
2014492118
Proceedings of the National Academy of Sciences
