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A Diagram of the procedure used for the CD16/32 passive immunotherapy. Neuropathological histology was performed in the SNpc (red square). B Representative confocal images showing the SNpc labeled with TH and counterstained with DAPI. Depletion of DA neurons can be appreciated in MPTP-treated animals. However, a protective effect can be seen in mice treated with CD16/32 neutralizing <t>monoclonal</t> antibodies (αCD16/32) (Scale bar: 30 μm). C Quantification of the DA neurons in the SNpc demonstrating a significant decrease in the MPTP group which is prevented by the administration of CD16/32 (*** p ˂0.001 MPTP vs. every treatment except MPTP + Isotype, ### p˂0.001 MPTP + Isotype vs. every treatment except MPTP). D 3D reconstruction of representative microglial cells expressing Iba-1 in different treatments of the experiment (Scale bar: 10 µm). E Quantification of the area of Iba-1 in the SNpc, indicating variation of microglial size when the animals were intoxicated with MPTP. F CD16/32 immunostaining reveals increased immunoreactivity in MPTP-treated animals (Scale bar: 20 μm). G Quantification of CD16/32 cell number shows increased levels in MPTP-treated animals. H Diagram of the procedure used for Cdc42 inhibition. I Representative confocal images of histological analysis. Upper panel: Representative images of TH positive neurons of the SNpc in every treatment (Scale bar: 30 µm). Lower panel: 3D reconstructions illustrating morphology and changes of size in microglial cells expressing Iba-1 (Scale bar: 10 µm). J Quantification of TH positive neurons indicating a significant decrease in the MPTP group and prevention by the previous administration of Cdc42 inhibitor ML141 (** p < 0.01 with respect to saline). K Quantification of the Iba-1 expressing area, which represents changes in microglial size. Microglial activation is present in the MPTP group evidenced by the increased area of Iba-1, which is decreased in the animals intoxicated with MPTP but previously treated with ML141 (*** p < 0.001 with respect to controls, $$ p < 0.01 with respect to ML141). L CD16/32 immunostaining reveals immunoreactivity in the MPTP group, providing a strong inhibition in MPTP-ML141 group (Scale bar: 30 μm). M Quantification of CD16/32+ microglia show a significant increase in the MPTP-treated group (** p < 0.01 compared to ML141 + MPTP).
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A Diagram of the procedure used for the CD16/32 passive immunotherapy. Neuropathological histology was performed in the SNpc (red square). B Representative confocal images showing the SNpc labeled with TH and counterstained with DAPI. Depletion of DA neurons can be appreciated in MPTP-treated animals. However, a protective effect can be seen in mice treated with CD16/32 neutralizing <t>monoclonal</t> antibodies (αCD16/32) (Scale bar: 30 μm). C Quantification of the DA neurons in the SNpc demonstrating a significant decrease in the MPTP group which is prevented by the administration of CD16/32 (*** p ˂0.001 MPTP vs. every treatment except MPTP + Isotype, ### p˂0.001 MPTP + Isotype vs. every treatment except MPTP). D 3D reconstruction of representative microglial cells expressing Iba-1 in different treatments of the experiment (Scale bar: 10 µm). E Quantification of the area of Iba-1 in the SNpc, indicating variation of microglial size when the animals were intoxicated with MPTP. F CD16/32 immunostaining reveals increased immunoreactivity in MPTP-treated animals (Scale bar: 20 μm). G Quantification of CD16/32 cell number shows increased levels in MPTP-treated animals. H Diagram of the procedure used for Cdc42 inhibition. I Representative confocal images of histological analysis. Upper panel: Representative images of TH positive neurons of the SNpc in every treatment (Scale bar: 30 µm). Lower panel: 3D reconstructions illustrating morphology and changes of size in microglial cells expressing Iba-1 (Scale bar: 10 µm). J Quantification of TH positive neurons indicating a significant decrease in the MPTP group and prevention by the previous administration of Cdc42 inhibitor ML141 (** p < 0.01 with respect to saline). K Quantification of the Iba-1 expressing area, which represents changes in microglial size. Microglial activation is present in the MPTP group evidenced by the increased area of Iba-1, which is decreased in the animals intoxicated with MPTP but previously treated with ML141 (*** p < 0.001 with respect to controls, $$ p < 0.01 with respect to ML141). L CD16/32 immunostaining reveals immunoreactivity in the MPTP group, providing a strong inhibition in MPTP-ML141 group (Scale bar: 30 μm). M Quantification of CD16/32+ microglia show a significant increase in the MPTP-treated group (** p < 0.01 compared to ML141 + MPTP).
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A Diagram of the procedure used for the CD16/32 passive immunotherapy. Neuropathological histology was performed in the SNpc (red square). B Representative confocal images showing the SNpc labeled with TH and counterstained with DAPI. Depletion of DA neurons can be appreciated in MPTP-treated animals. However, a protective effect can be seen in mice treated with CD16/32 neutralizing <t>monoclonal</t> antibodies (αCD16/32) (Scale bar: 30 μm). C Quantification of the DA neurons in the SNpc demonstrating a significant decrease in the MPTP group which is prevented by the administration of CD16/32 (*** p ˂0.001 MPTP vs. every treatment except MPTP + Isotype, ### p˂0.001 MPTP + Isotype vs. every treatment except MPTP). D 3D reconstruction of representative microglial cells expressing Iba-1 in different treatments of the experiment (Scale bar: 10 µm). E Quantification of the area of Iba-1 in the SNpc, indicating variation of microglial size when the animals were intoxicated with MPTP. F CD16/32 immunostaining reveals increased immunoreactivity in MPTP-treated animals (Scale bar: 20 μm). G Quantification of CD16/32 cell number shows increased levels in MPTP-treated animals. H Diagram of the procedure used for Cdc42 inhibition. I Representative confocal images of histological analysis. Upper panel: Representative images of TH positive neurons of the SNpc in every treatment (Scale bar: 30 µm). Lower panel: 3D reconstructions illustrating morphology and changes of size in microglial cells expressing Iba-1 (Scale bar: 10 µm). J Quantification of TH positive neurons indicating a significant decrease in the MPTP group and prevention by the previous administration of Cdc42 inhibitor ML141 (** p < 0.01 with respect to saline). K Quantification of the Iba-1 expressing area, which represents changes in microglial size. Microglial activation is present in the MPTP group evidenced by the increased area of Iba-1, which is decreased in the animals intoxicated with MPTP but previously treated with ML141 (*** p < 0.001 with respect to controls, $$ p < 0.01 with respect to ML141). L CD16/32 immunostaining reveals immunoreactivity in the MPTP group, providing a strong inhibition in MPTP-ML141 group (Scale bar: 30 μm). M Quantification of CD16/32+ microglia show a significant increase in the MPTP-treated group (** p < 0.01 compared to ML141 + MPTP).
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A Diagram of the procedure used for the CD16/32 passive immunotherapy. Neuropathological histology was performed in the SNpc (red square). B Representative confocal images showing the SNpc labeled with TH and counterstained with DAPI. Depletion of DA neurons can be appreciated in MPTP-treated animals. However, a protective effect can be seen in mice treated with CD16/32 neutralizing monoclonal antibodies (αCD16/32) (Scale bar: 30 μm). C Quantification of the DA neurons in the SNpc demonstrating a significant decrease in the MPTP group which is prevented by the administration of CD16/32 (*** p ˂0.001 MPTP vs. every treatment except MPTP + Isotype, ### p˂0.001 MPTP + Isotype vs. every treatment except MPTP). D 3D reconstruction of representative microglial cells expressing Iba-1 in different treatments of the experiment (Scale bar: 10 µm). E Quantification of the area of Iba-1 in the SNpc, indicating variation of microglial size when the animals were intoxicated with MPTP. F CD16/32 immunostaining reveals increased immunoreactivity in MPTP-treated animals (Scale bar: 20 μm). G Quantification of CD16/32 cell number shows increased levels in MPTP-treated animals. H Diagram of the procedure used for Cdc42 inhibition. I Representative confocal images of histological analysis. Upper panel: Representative images of TH positive neurons of the SNpc in every treatment (Scale bar: 30 µm). Lower panel: 3D reconstructions illustrating morphology and changes of size in microglial cells expressing Iba-1 (Scale bar: 10 µm). J Quantification of TH positive neurons indicating a significant decrease in the MPTP group and prevention by the previous administration of Cdc42 inhibitor ML141 (** p < 0.01 with respect to saline). K Quantification of the Iba-1 expressing area, which represents changes in microglial size. Microglial activation is present in the MPTP group evidenced by the increased area of Iba-1, which is decreased in the animals intoxicated with MPTP but previously treated with ML141 (*** p < 0.001 with respect to controls, $$ p < 0.01 with respect to ML141). L CD16/32 immunostaining reveals immunoreactivity in the MPTP group, providing a strong inhibition in MPTP-ML141 group (Scale bar: 30 μm). M Quantification of CD16/32+ microglia show a significant increase in the MPTP-treated group (** p < 0.01 compared to ML141 + MPTP).

Journal: NPJ Parkinson's Disease

Article Title: Microglial low-affinity FcγR mediates the phagocytic elimination of dopaminergic neurons in Parkinson’s disease degeneration

doi: 10.1038/s41531-025-01249-9

Figure Lengend Snippet: A Diagram of the procedure used for the CD16/32 passive immunotherapy. Neuropathological histology was performed in the SNpc (red square). B Representative confocal images showing the SNpc labeled with TH and counterstained with DAPI. Depletion of DA neurons can be appreciated in MPTP-treated animals. However, a protective effect can be seen in mice treated with CD16/32 neutralizing monoclonal antibodies (αCD16/32) (Scale bar: 30 μm). C Quantification of the DA neurons in the SNpc demonstrating a significant decrease in the MPTP group which is prevented by the administration of CD16/32 (*** p ˂0.001 MPTP vs. every treatment except MPTP + Isotype, ### p˂0.001 MPTP + Isotype vs. every treatment except MPTP). D 3D reconstruction of representative microglial cells expressing Iba-1 in different treatments of the experiment (Scale bar: 10 µm). E Quantification of the area of Iba-1 in the SNpc, indicating variation of microglial size when the animals were intoxicated with MPTP. F CD16/32 immunostaining reveals increased immunoreactivity in MPTP-treated animals (Scale bar: 20 μm). G Quantification of CD16/32 cell number shows increased levels in MPTP-treated animals. H Diagram of the procedure used for Cdc42 inhibition. I Representative confocal images of histological analysis. Upper panel: Representative images of TH positive neurons of the SNpc in every treatment (Scale bar: 30 µm). Lower panel: 3D reconstructions illustrating morphology and changes of size in microglial cells expressing Iba-1 (Scale bar: 10 µm). J Quantification of TH positive neurons indicating a significant decrease in the MPTP group and prevention by the previous administration of Cdc42 inhibitor ML141 (** p < 0.01 with respect to saline). K Quantification of the Iba-1 expressing area, which represents changes in microglial size. Microglial activation is present in the MPTP group evidenced by the increased area of Iba-1, which is decreased in the animals intoxicated with MPTP but previously treated with ML141 (*** p < 0.001 with respect to controls, $$ p < 0.01 with respect to ML141). L CD16/32 immunostaining reveals immunoreactivity in the MPTP group, providing a strong inhibition in MPTP-ML141 group (Scale bar: 30 μm). M Quantification of CD16/32+ microglia show a significant increase in the MPTP-treated group (** p < 0.01 compared to ML141 + MPTP).

Article Snippet: anti-Cdc42 , mouse monoclonal , 1:500 , 2 mg/mL , Cytoskeleton [ACD03-A].

Techniques: Labeling, Bioprocessing, Expressing, Immunostaining, Inhibition, Saline, Activation Assay