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The actin remodeling protein cofilin is crucial for thymic αβ but not γδ T-cell development

Seeland, Isabel, Xiong, Ying, Orlik, Christian, Deibel, Daniel, Prokosch, Sandra, Küblbeck, Günter, Jahraus, Beate, De Stefano, Daniela, Moos, Sonja, Kurschus, Florian C., Arnold, Bernd, Samstag, Yvonne·2018·PLOS Biology
DOI 10.1371/journal.pbio.2005380PMC PMC6053251
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Fig 1 Cofilin expressed from an eGFP-2A-Cfl1 cassette is not functional in T-cells. Jurkat T cells were either transfected with no siRNA (mock), a nontargeting control siRNA or a cofilin-specific siRNA (binding to the 3′ UTR), in order to downregulate endogenous cofilin. Some of the cells that received cofilin siRNA were cotransfected with Cfl1-eGFP control vector or a vector carrying the eGFP-2A-Cfl1 sequence under the control of the CMV promoter. Cells were harvested and analyzed 48 h after transfection. (A) Exemplary flow cytometric analysis of eGFP expression of transfected Jurkat cells (n = 4 independent experiments). (B) Western blot analysis of total cell lysates by staining for total cofilin and GAPDH. All samples were normalized to cells transfected with cofilin siRNA, which was set as 1. Data is represented as mean ± SEM (n = 4 independent experiments). (C) Exemplary western blot showing pCfl1, total Cfl1, and control GAPDH staining. Endogenous cofilin has a size of 19 kDa (lanes 1–3 and 5), whereas cofilin derived from the Cfl1-eGFP control vector is expressed as eGFP fusion protein (size: 46 kDa, lane 4). (D) Total cellular F-actin content was analyzed by flow cytometric measurement of phalloidin binding. All samples were normalized to cells transfected with cofilin siRNA. Data is represented as mean ± SEM (n = 3 independent experiments). Significances were calculated against Jurkat cells transfected with siRNA only. ** p < 0.01; * p < 0.05. Underlying data can be found in S1 Data. Cfl1, cofilin-1; CMV, cytomegalovirus; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; ns, not significant.
Fig 1 Cofilin expressed from an eGFP-2A-Cfl1 cassette is not functional in T-cells. Jurkat T cells were either transfected with no siRNA (mock), a nontargeting control siRNA or a cofilin-specific siRNA (binding to the 3′ UTR), in order to downregulate endogenous cofilin. Some of the cells that received cofilin siRNA were cotransfected with Cfl1-eGFP control vector or a vector carrying the eGFP-2A-Cfl1 sequence under the control of the CMV promoter. Cells were harvested and analyzed 48 h after transfection. (A) Exemplary flow cytometric analysis of eGFP expression of transfected Jurkat cells (n = 4 independent experiments). (B) Western blot analysis of total cell lysates by staining for total cofilin and GAPDH. All samples were normalized to cells transfected with cofilin siRNA, which was set as 1. Data is represented as mean ± SEM (n = 4 independent experiments). (C) Exemplary western blot showing pCfl1, total Cfl1, and control GAPDH staining. Endogenous cofilin has a size of 19 kDa (lanes 1–3 and 5), whereas cofilin derived from the Cfl1-eGFP control vector is expressed as eGFP fusion protein (size: 46 kDa, lane 4). (D) Total cellular F-actin content was analyzed by flow cytometric measurement of phalloidin binding. All samples were normalized to cells transfected with cofilin siRNA. Data is represented as mean ± SEM (n = 3 independent experiments). Significances were calculated against Jurkat cells transfected with siRNA only. ** p < 0.01; * p < 0.05. Underlying data can be found in S1 Data. Cfl1, cofilin-1; CMV, cytomegalovirus; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; ns, not significant.CC BY · PubMed Central
Fig 2 Mice expressing nf cofilin show a severe thymus atrophy and a developmental arrest at the DN3 stage. (A) Total T-cell number in spleen of B6 mice and nf cofilin knock-in mice (n = 6 independent experiments with a total of ≥8 mice per group). (B) Thymus was isolated and weighed, and the total cell number was determined from 4–5-weeks-old B6 or nf cofilin knock-in mice (n = 6 independent experiments with a total of ≥10 mice per group). (C) Flow cytometric analysis of thymocyte differentiation by CD4, CD8, CD25, and CD44 staining (n ≥ 8 mice per group). Exemplary dot blots from representative mice are shown on the left, whereas the statistical evaluation of summary data is shown in the middle (for DN, DP, and SP stages) and on the right (for DN cell stages). (D) Creation of mixed bone marrow chimera. Lethally irradiated B6 mice were reconstituted with equal numbers of CD3+ cell–depleted BM cells from CD45.2+ tester (Cfl1nf/nf) and CD45.1+ competitor (B6) mice. Total chimerism was measured and CD4 versus CD8 plots show the developmental stage of thymocytes derived from CD45.1+ or CD45.2+ BM cells. Plots are representative of six mixed chimeras per group. Bar graphs show the average abundance of each major thymocyte population within the chimera from both tester (CD45.2+) and competitor (CD45.1+) donor cells. Data is represented as mean ± SEM. **** = p<0.0001; ** = p<0.01. Underlying Data can be found in S1 Data. BM, bone marrow; DN, double negative; DP, double positive; SP, single positive.
Fig 2 Mice expressing nf cofilin show a severe thymus atrophy and a developmental arrest at the DN3 stage. (A) Total T-cell number in spleen of B6 mice and nf cofilin knock-in mice (n = 6 independent experiments with a total of ≥8 mice per group). (B) Thymus was isolated and weighed, and the total cell number was determined from 4–5-weeks-old B6 or nf cofilin knock-in mice (n = 6 independent experiments with a total of ≥10 mice per group). (C) Flow cytometric analysis of thymocyte differentiation by CD4, CD8, CD25, and CD44 staining (n ≥ 8 mice per group). Exemplary dot blots from representative mice are shown on the left, whereas the statistical evaluation of summary data is shown in the middle (for DN, DP, and SP stages) and on the right (for DN cell stages). (D) Creation of mixed bone marrow chimera. Lethally irradiated B6 mice were reconstituted with equal numbers of CD3+ cell–depleted BM cells from CD45.2+ tester (Cfl1nf/nf) and CD45.1+ competitor (B6) mice. Total chimerism was measured and CD4 versus CD8 plots show the developmental stage of thymocytes derived from CD45.1+ or CD45.2+ BM cells. Plots are representative of six mixed chimeras per group. Bar graphs show the average abundance of each major thymocyte population within the chimera from both tester (CD45.2+) and competitor (CD45.1+) donor cells. Data is represented as mean ± SEM. **** = p<0.0001; ** = p<0.01. Underlying Data can be found in S1 Data. BM, bone marrow; DN, double negative; DP, double positive; SP, single positive.CC BY · PubMed Central
Fig 3 DN thymocytes of Cfl1nf/nf mice show a dramatically enhanced F-actin content and impaired migratory capacity as well as a lack of TCRβ surface expression. (A) CD3+ splenocytes were analyzed for expression of TCRβ and TCRγδ. Shown are representative dot blots (left panels) and calculated absolute cell numbers (right panel) of TCRβ and TCRγδ expressing cells. Data is represented as mean ± SEM and summarizes 3 independent experiments with a total of 6 mice per group. (B) Total F-actin amount of DN thymocytes or γδ thymocytes was determined by SiR-actin staining (n = 3 independent experiments with a total ≥6 mice per group). (C) Migratory capacity of DN cells or γδ thymocytes was determined in a transwell assay (pore size 5 μm) in which SDF-1α (200 ng/ml) was used as chemotactic stimulus. Migration was carried out for 3 h (n = 3 independent experiments with ≥4 mice per group). (D) TCRβ surface (surface TCRβ) and intracellular (ic TCRβ) expression was analyzed in DN cells by flow cytometry. Representative dot plots from TCRβ versus TCRγδ staining on B6 and Cfl1nf/nf DN cells are shown (n = 4 independent experiments with a total of ≥7 mice per group). (E) Analysis of surface and ic expression of TCRβ in DN cells of B6 (grey bar) and Cfl1nf/nf mice (black bar) (left bar chart). Analysis of MFI of TCRβ of icTCRβ+ DN cells of B6 (grey bar) and Cfl1nf/nf mice (black bar) (right bar chart). (F) Analysis of surface expression of TCRβ in DN thymocytes of B6 and Cfl1nf/nf mice before (-cytoD) and after cytochalasin D treatment (+cytoD). Data is represented as mean ± SEM. **** p < 0.0001; *** p < 0.001; ** p < 0.01; * p < 0.05; Underlying data can be found in S1 Data. cytoD, cytochalasin D; ic, intracellular; MFI, mean fluorescence intensity nf, nonfunctional; ns, not significant.
Fig 3 DN thymocytes of Cfl1nf/nf mice show a dramatically enhanced F-actin content and impaired migratory capacity as well as a lack of TCRβ surface expression. (A) CD3+ splenocytes were analyzed for expression of TCRβ and TCRγδ. Shown are representative dot blots (left panels) and calculated absolute cell numbers (right panel) of TCRβ and TCRγδ expressing cells. Data is represented as mean ± SEM and summarizes 3 independent experiments with a total of 6 mice per group. (B) Total F-actin amount of DN thymocytes or γδ thymocytes was determined by SiR-actin staining (n = 3 independent experiments with a total ≥6 mice per group). (C) Migratory capacity of DN cells or γδ thymocytes was determined in a transwell assay (pore size 5 μm) in which SDF-1α (200 ng/ml) was used as chemotactic stimulus. Migration was carried out for 3 h (n = 3 independent experiments with ≥4 mice per group). (D) TCRβ surface (surface TCRβ) and intracellular (ic TCRβ) expression was analyzed in DN cells by flow cytometry. Representative dot plots from TCRβ versus TCRγδ staining on B6 and Cfl1nf/nf DN cells are shown (n = 4 independent experiments with a total of ≥7 mice per group). (E) Analysis of surface and ic expression of TCRβ in DN cells of B6 (grey bar) and Cfl1nf/nf mice (black bar) (left bar chart). Analysis of MFI of TCRβ of icTCRβ+ DN cells of B6 (grey bar) and Cfl1nf/nf mice (black bar) (right bar chart). (F) Analysis of surface expression of TCRβ in DN thymocytes of B6 and Cfl1nf/nf mice before (-cytoD) and after cytochalasin D treatment (+cytoD). Data is represented as mean ± SEM. **** p < 0.0001; *** p < 0.001; ** p < 0.01; * p < 0.05; Underlying data can be found in S1 Data. cytoD, cytochalasin D; ic, intracellular; MFI, mean fluorescence intensity nf, nonfunctional; ns, not significant.CC BY · PubMed Central
Fig 4 Cfl1nf/nf mice show normal γδ T-cell subsets which remain functional. (A) Analysis of the surface expression of Vγ1, Vγ2, and Vγ3 of γδ T-cells isolated from the spleen, skin, lung, and thymus of B6 (grey bar) or Cfl1nf/nf mice (black bar) (n = 4 independent experiments with ≥4 mice per group). (B) Analysis of the surface expression of CD24, CD27, and CD44 of γδ thymocytes of B6 (grey bar) or Cfl1nf/nf mice (black bar) (n = 4 independent experiments with ≥4 mice per group). (C) In vitro activation of splenic γδ T cells of Cfl1nf/nf (black bar) and control mice (grey bar) by plate-bound CD3 and CD28 antibodies for 24 h. Determination of the T-cell activation markers CD25 (left bar chart) and CD69 (right bar chart) by flow cytometry. (D) Age- and sex-matched Cfl1nf/nf (red line) and Cfl1+/+ (black line) mice at 7 weeks of age were used for an IMQ-induced psoriasis-like model. Over 6 days, prior to topical application of IMQ, scores of individual parameters such as scaling, back skin thickness, and erythema formation were measured and the accumulated PASI was calculated. (E) Flow cytometric analysis of IL-17A and RORγt expression in γδ T cells of skin-draining LNs. Cytokine production was assessed after 6 days of topical application of IMQ containing Aldara crème (Sham) or control crème (Aldara) (experiment with ≥4 mice per group). Data are represented as mean ± SEM. **** p < 0.0001; *** p < 0.001; ** p < 0.01; * p < 0.05; Underlying data can be found in S1 Data. Cfl1, cofilin-1; IMQ, imiquimod; ns, not significant; PASI, psoriasis area severity index.
Fig 4 Cfl1nf/nf mice show normal γδ T-cell subsets which remain functional. (A) Analysis of the surface expression of Vγ1, Vγ2, and Vγ3 of γδ T-cells isolated from the spleen, skin, lung, and thymus of B6 (grey bar) or Cfl1nf/nf mice (black bar) (n = 4 independent experiments with ≥4 mice per group). (B) Analysis of the surface expression of CD24, CD27, and CD44 of γδ thymocytes of B6 (grey bar) or Cfl1nf/nf mice (black bar) (n = 4 independent experiments with ≥4 mice per group). (C) In vitro activation of splenic γδ T cells of Cfl1nf/nf (black bar) and control mice (grey bar) by plate-bound CD3 and CD28 antibodies for 24 h. Determination of the T-cell activation markers CD25 (left bar chart) and CD69 (right bar chart) by flow cytometry. (D) Age- and sex-matched Cfl1nf/nf (red line) and Cfl1+/+ (black line) mice at 7 weeks of age were used for an IMQ-induced psoriasis-like model. Over 6 days, prior to topical application of IMQ, scores of individual parameters such as scaling, back skin thickness, and erythema formation were measured and the accumulated PASI was calculated. (E) Flow cytometric analysis of IL-17A and RORγt expression in γδ T cells of skin-draining LNs. Cytokine production was assessed after 6 days of topical application of IMQ containing Aldara crème (Sham) or control crème (Aldara) (experiment with ≥4 mice per group). Data are represented as mean ± SEM. **** p < 0.0001; *** p < 0.001; ** p < 0.01; * p < 0.05; Underlying data can be found in S1 Data. Cfl1, cofilin-1; IMQ, imiquimod; ns, not significant; PASI, psoriasis area severity index.CC BY · PubMed Central

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Metadata

Authors
Seeland, I., Xiong, Y., Orlik, C., Deibel, D., Prokosch, S., Küblbeck, G., Jahraus, B., De Stefano, D., Moos, S., Kurschus, F. C., Arnold, B., & Samstag, Y.
Venue
PLOS Biology
Publisher
Public Library of Science (PLoS)
Published
2018-07-09
Volume
16
Issue
7
Pages
e2005380
ISSN
1545-7885
DOI
10.1371/journal.pbio.2005380
PMC
PMC6053251
Cited by
12
References
2
Language
en
Update notices
new_version (2018-07-19)
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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