CCL21 ELISA Kits Search Results


anti-ccl21  (Becton Dickinson)
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Becton Dickinson anti-ccl21
CCR7 plays a dual role in DCs mobilization, promoting chemotaxis and docking to lymphatics. After s.c. injection of LPS-activated CFSE-stained BMDCs to the footpad, WT DCs (a–c) moved linearly toward an initial lymphatic, compatible with chemotaxis. DCs that crossed the endothelium clustered in the proximal sections of initial lymphatics, either in blind ends (c, left rectangle) or in adjacent sections (c, right rectangle). (d) Within 24 h, WT cells have efficiently entered lymphatics. In contrast, CCR7 −/− cells (e) kept crawling in the interstitium bypassing the lymphatic vessels they encountered (four representative cells tracked), suggesting that CCR7 promotes DC adhesion to lymphatics. This pattern was also apparent (f) when both WT and CCR7 −/− DCs were co-injected. CCR7 −/− DCs crawled as fast as WT DCs in the dermis (P = 0.29; g) but were less persistent (P = 0.006; h), implying that CCR7 ligation is not essential for DC chemokinesis but participates in their chemotaxis. Persistence index was calculated by dividing the cell displacement by path length. Data points represent individual cells and were pooled from three mice for each condition. Red bars denote the mean. *, P = 0.006. (i) When BMDCs were co-injected with <t>CCL21,</t> their migration to the popliteal LN was not affected, indicating that misplaced chemokine did not misguide DCs and prevent random migration and docking on endothelial <t>CCL21.</t> Data indicate the percentage of injected DCs out of resident LN CD11c + cells. Error bars denote SEM.
Anti Ccl21, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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CCR7 plays a dual role in DCs mobilization, promoting chemotaxis and docking to lymphatics. After s.c. injection of LPS-activated CFSE-stained BMDCs to the footpad, WT DCs (a–c) moved linearly toward an initial lymphatic, compatible with chemotaxis. DCs that crossed the endothelium clustered in the proximal sections of initial lymphatics, either in blind ends (c, left rectangle) or in adjacent sections (c, right rectangle). (d) Within 24 h, WT cells have efficiently entered lymphatics. In contrast, CCR7 −/− cells (e) kept crawling in the interstitium bypassing the lymphatic vessels they encountered (four representative cells tracked), suggesting that CCR7 promotes DC adhesion to lymphatics. This pattern was also apparent (f) when both WT and CCR7 −/− DCs were co-injected. CCR7 −/− DCs crawled as fast as WT DCs in the dermis (P = 0.29; g) but were less persistent (P = 0.006; h), implying that CCR7 ligation is not essential for DC chemokinesis but participates in their chemotaxis. Persistence index was calculated by dividing the cell displacement by path length. Data points represent individual cells and were pooled from three mice for each condition. Red bars denote the mean. *, P = 0.006. (i) When BMDCs were co-injected with CCL21, their migration to the popliteal LN was not affected, indicating that misplaced chemokine did not misguide DCs and prevent random migration and docking on endothelial CCL21. Data indicate the percentage of injected DCs out of resident LN CD11c + cells. Error bars denote SEM.

Journal: The Journal of Experimental Medicine

Article Title: DC mobilization from the skin requires docking to immobilized CCL21 on lymphatic endothelium and intralymphatic crawling

doi: 10.1084/jem.20102392

Figure Lengend Snippet: CCR7 plays a dual role in DCs mobilization, promoting chemotaxis and docking to lymphatics. After s.c. injection of LPS-activated CFSE-stained BMDCs to the footpad, WT DCs (a–c) moved linearly toward an initial lymphatic, compatible with chemotaxis. DCs that crossed the endothelium clustered in the proximal sections of initial lymphatics, either in blind ends (c, left rectangle) or in adjacent sections (c, right rectangle). (d) Within 24 h, WT cells have efficiently entered lymphatics. In contrast, CCR7 −/− cells (e) kept crawling in the interstitium bypassing the lymphatic vessels they encountered (four representative cells tracked), suggesting that CCR7 promotes DC adhesion to lymphatics. This pattern was also apparent (f) when both WT and CCR7 −/− DCs were co-injected. CCR7 −/− DCs crawled as fast as WT DCs in the dermis (P = 0.29; g) but were less persistent (P = 0.006; h), implying that CCR7 ligation is not essential for DC chemokinesis but participates in their chemotaxis. Persistence index was calculated by dividing the cell displacement by path length. Data points represent individual cells and were pooled from three mice for each condition. Red bars denote the mean. *, P = 0.006. (i) When BMDCs were co-injected with CCL21, their migration to the popliteal LN was not affected, indicating that misplaced chemokine did not misguide DCs and prevent random migration and docking on endothelial CCL21. Data indicate the percentage of injected DCs out of resident LN CD11c + cells. Error bars denote SEM.

Article Snippet: The antibodies used were directed against LYVE-1 and CCL21 (as in the previous paragraph), VE-cadherin (rat clone 11D4.1; BD), Collagen IV (rabbit polyclonal; Cosmobio), and MHCII (rat clone M5/114.15.2; eBioscience).

Techniques: Chemotaxis Assay, Injection, Staining, Ligation, Migration

CCL21 depositions are concentrated in specific regions of LECs. Whole-mount confocal images of the skin of the footpad (a) or ear (b) stained for LYVE-1 and CCL21 showed a punctate expression of CCL21 on initial lymphatics (blue dots). (c) This pattern was even more obvious after isosurface rendering. (d and e) Triple staining for VE-cadherin, LYVE-1, and CCL21 shows alternate arrangement of VE-cadherin at button junctions and LYVE-1 at loose flaps. CCL21 puncta are located in the junction-free areas of the LECs. (f–h) Compared with the steady-state, inflammation, either through CHS (g) or CFA (h), did not affect the pattern of CCL21 puncta or increase the CCL21 signal after 24 h.

Journal: The Journal of Experimental Medicine

Article Title: DC mobilization from the skin requires docking to immobilized CCL21 on lymphatic endothelium and intralymphatic crawling

doi: 10.1084/jem.20102392

Figure Lengend Snippet: CCL21 depositions are concentrated in specific regions of LECs. Whole-mount confocal images of the skin of the footpad (a) or ear (b) stained for LYVE-1 and CCL21 showed a punctate expression of CCL21 on initial lymphatics (blue dots). (c) This pattern was even more obvious after isosurface rendering. (d and e) Triple staining for VE-cadherin, LYVE-1, and CCL21 shows alternate arrangement of VE-cadherin at button junctions and LYVE-1 at loose flaps. CCL21 puncta are located in the junction-free areas of the LECs. (f–h) Compared with the steady-state, inflammation, either through CHS (g) or CFA (h), did not affect the pattern of CCL21 puncta or increase the CCL21 signal after 24 h.

Article Snippet: The antibodies used were directed against LYVE-1 and CCL21 (as in the previous paragraph), VE-cadherin (rat clone 11D4.1; BD), Collagen IV (rabbit polyclonal; Cosmobio), and MHCII (rat clone M5/114.15.2; eBioscience).

Techniques: Staining, Expressing

CCL21 immobilization on the basement membrane of initial lymphatics may facilitate DC adhesion at CCL21-rich sites and passage through dedicated portals. (a) Collagen IV staining in whole-mount preparations of the ear skin shows perforations within the basement membrane of initial lymphatics (arrows in boxed region). (b) CCL21 staining reveals that several, but not all, of these perforations (arrows) are associated with CCL21 puncta. (c) Treatment of skin cross sections with type IV collagenase digested the basal membrane of initial lymphatics, markedly reducing collagen on lymphatics. Membrane-bound CCL21was dissociated, leaving behind small perinuclear depositions (arrows). (d) In the presence of the calcium chelator EDTA, collagenase IV treatment did not disrupt collagen (left) and CCL21 (right). (e–h) 24 h after contact sensitization, skin whole mounts were triple-stained for LYVE-1, CCL21, and MHC-II. MHC-II + DCs accumulated outside initial lymphatics (e). (f) Enlargement of the boxed region in e shows in three dimensions a DC which extended protrusions toward the initial lymphatic vessel and contacted two CCL21-rich puncta. Two other examples of DCs contacting CCL21 are shown (g and h). (i–l) Similar results were obtained when the skin of CD11c-EYFP mice was analyzed. Collectively, these findings suggest that CCL21 is secreted from intracellular stores inside LECs and is immobilized on the basal membrane (often near preformed portals), to promote DC adhesion and site-specific transmigration.

Journal: The Journal of Experimental Medicine

Article Title: DC mobilization from the skin requires docking to immobilized CCL21 on lymphatic endothelium and intralymphatic crawling

doi: 10.1084/jem.20102392

Figure Lengend Snippet: CCL21 immobilization on the basement membrane of initial lymphatics may facilitate DC adhesion at CCL21-rich sites and passage through dedicated portals. (a) Collagen IV staining in whole-mount preparations of the ear skin shows perforations within the basement membrane of initial lymphatics (arrows in boxed region). (b) CCL21 staining reveals that several, but not all, of these perforations (arrows) are associated with CCL21 puncta. (c) Treatment of skin cross sections with type IV collagenase digested the basal membrane of initial lymphatics, markedly reducing collagen on lymphatics. Membrane-bound CCL21was dissociated, leaving behind small perinuclear depositions (arrows). (d) In the presence of the calcium chelator EDTA, collagenase IV treatment did not disrupt collagen (left) and CCL21 (right). (e–h) 24 h after contact sensitization, skin whole mounts were triple-stained for LYVE-1, CCL21, and MHC-II. MHC-II + DCs accumulated outside initial lymphatics (e). (f) Enlargement of the boxed region in e shows in three dimensions a DC which extended protrusions toward the initial lymphatic vessel and contacted two CCL21-rich puncta. Two other examples of DCs contacting CCL21 are shown (g and h). (i–l) Similar results were obtained when the skin of CD11c-EYFP mice was analyzed. Collectively, these findings suggest that CCL21 is secreted from intracellular stores inside LECs and is immobilized on the basal membrane (often near preformed portals), to promote DC adhesion and site-specific transmigration.

Article Snippet: The antibodies used were directed against LYVE-1 and CCL21 (as in the previous paragraph), VE-cadherin (rat clone 11D4.1; BD), Collagen IV (rabbit polyclonal; Cosmobio), and MHCII (rat clone M5/114.15.2; eBioscience).

Techniques: Staining, Transmigration Assay