EMBO/soda-nel huggingface dataset:
Targeting gut dysbiosis against inflammation and impaired autophagy in Duchenne muscular dystrophy (2022)
Figure 10

Figure 10. Effect of NaB, MK1903 and Rosiglitazone in primary myoblasts isolated from DMD

donors.

A-E Bar chart showing the mRNA expression levels of IL6, COX2, ULK 1, ATG13 and ATG4 mRNA in primary human myoblasts isolated from one healthy donor (HD) and five DMD donors (D1- D5).

Data Information: The quantification of transcripts by quantitative real-time PCR was measured twice for each sample.
Molecular profiling reveals features of clinical immunity and immunosuppression in asymptomatic P. falciparum malaria (2022)
Figure 2

Figure 2. Identification of MBC and memory CD4+ T cell sub-populations induced by P. falciparum symptomatic and asymptomatic infection.

PBMCs from P. falciparum symptomatic (n=16) and asymptomatic (n=24) infected individuals as well as healthy immune controls (n=24) were stained with a panel of metal-labelled antibodies and analysed by CyTOF. tSNE analysis was performed and FlowSOM clustering was used to identify individual cell sub-populations within gated:

A. TH1-like memory CD4+ T cells (CD19-CD3+CD4+CD45RA-CCR6-CXCR3+)

B. TH2-like memory CD4+ T cells (CD19-CD3+CD4+CD45RA-CCR6-CXCR3-)

C. Circulating memory TFH cells (CD19-CD3+CD4+CD45RA-CXCR5+)

D. Classical MBCs (CD3-CD19+CD20+CD10-CD27+CD21+)

E. Atypical MBCs (CD3-CD19+CD20+CD10-CD27-CD21-)

F. Activated MBCs (CD3-CD19+CD20+CD10-CD27+CD21-)

The tSNE plots in the top panel display cell density and represent the pooled data for each group, while the lower panel shows a projection of the FlowSOM clusters on a tSNE plot. Heatmaps show the median marker expression for each FlowSOM cluster.
Molecular profiling reveals features of clinical immunity and immunosuppression in asymptomatic P. falciparum malaria (2022)
Figure 8

Figure 8. Asymptomatic P. falciparum malaria supports humoral responses to infection but drives immunosuppressive responses.

A. Volcano plot showing genes upregulated in symptomatic individuals that were significantly correlated with IgM+ activated MBCs.

B. Volcano plot showing genes upregulated in symptomatic individuals that were significantly correlated with T-bet+ CD4+ T cells.

C. Chord diagram integrating associations between symptomatic malaria signature genes, immune cell populations and antibody responses. Blue lines within the chord diagram represent positive correlations between two variables, while red lines represent negative correlations. (Benjamini-Hochberg adjusted Spearman's Rho, FDR<5%).

D. Chord diagram integrating associations between asymptomatic malaria signature genes, immune cell populations and antibody responses. Blue lines within the chord diagram represent positive correlations between two variables, while red lines represent negative correlations. (Benjamini-Hochberg adjusted Spearman's Rho, FDR<5%).
Molecular profiling reveals features of clinical immunity and immunosuppression in asymptomatic P. falciparum malaria (2022)
Figure 9

Figure 9. CTLA-4 is upregulated in memory CD4+ T cells in asymptomatic malaria and contributes to the development of clinically-silent parasitemia.

A. Estimated proportions of PBMC subpopulations determined from cell-type deconvolution featuring transcriptional profiles upregulated in asymptomatic individuals.

B-G. PBMCs from P. falciparum symptomatic (n=6) and asymptomatic (n=6) infected individuals as well as healthy immune controls (n=6) were stained with a panel of antibodies and analyzed by flow cytometry. tSNE plots (B) display cell density of the pooled data for each group, (C) shows a projection of the FlowSOM clusters on a tSNE plot, and (D) is a heatmap depicting the celluar phenotype of clusters of CTLA-4+CD3+CD19- cells. Bar plots representing mean relative abundance of biological replicates + SEM of relevant clusters among clinical groups (E), Mann-Whitney test, *p<0.05. The panel on the left shows the average CTLA-4 mean fluorescent intensity (MFI) or 6 biological replicates in cluster 4 + SEM, Mann-Whitney test, **p<0.01, while representative histograms of CTLA-4 expression in cluster 4 are shown on the right (F). Marker intensity within clusters 1 and 6 (G).

H. C57BL/6 mice (n=10) were infected with P. chabaudi chabaudi. Percentage parasitemia of infected mice was determined every 2-3 days. Symbols represent average parasitemia + SEM.

I-Q. Splenocytes from P. chabaudi chabaudi infected mice were stained with fluorescent antibodies and analyzed by flow cytometry. (I) Representative contour plots showing CTLA-4-expressing cells among TREG and CD44+ CD4+ T cells. (J, K) Percentage of CTLA-4+ cells among CD4+FoxP3+ Treg cells (J) and CD44+ activated CD4+ T cells (K) at peak (day 8 p.i) and recrudescent (day 20 p.i) parasitemia and after infection resolution (day 40 p.i). Bar plots represent mean percentage of 6 biological replicates + SEM (unpaired t-test, ***p<0.005, *p<0.05). (L-N) tSNE plots (L) display cell density of the pooled data for each group, (M) shows a projection of the FlowSOM clusters on a tSNE plot, and (N) is a heatmap depicting the celluar phenotype of CTLA-4+ conventional CD4+ T cells during peak and recrudescent parasitemia. (O) Bar plots represent the average relative abundance of 6 biological replicates in relevant clusters + SEM (unpaired t-test, **p<0.01). (P-Q) Representative contour plots (P) and absolute number (Q) of CTLA-4-expressing CD4+CD44+CCR7+CD62Lhigh central memory (CM) and CD4+CD44+CCR7-CD62Llow effector memory (EM) cells during peak and recrudescent parasitemia. Symbols represent the mean cell number of 6 biological replicates + SEM (unpaired t-test, ***p<0.05).

R. C57BL/6 mice (n=6) were infected with P. chabaudi chabaudi and treated with anti-CTLA-4 or isotype control every 3 days from day 13 p.i as indicated by the red arrows. Parasitemia was determined every 2-3 days. Bar plots represent mean parasitemia of biological replicates + SEM (unpaired t-test, **p<0.01, *p<0.05).

Expanded View Figure Legends
sTREM2 is associated with amyloid-related p-tau increases and glucose hypermetabolism in Alzheimer's (2022)
Figure 1

Figure 1. Cross-sectional and longitudinal analysis of the association between amyloid-PET (in centiloid), CSF p-tau181, and CSF sTREM2 in early Aβ-accumulators (i.e. Aβ CSF+/PET−; n=70) and late Aβ-accumulators (i.e. Aβ CSF+/PET+; n=201). Cross-sectional linear regressions between A) centiloid and p-tau181 and B) centiloid and sTREM2. Longitudinal linear regressions between C) centiloid and change in p-tau181 and D) centiloid and change in sTREM2. Standardized beta-estimates (β), T-values, and p-values were derived from linear regressions controlling for age, sex, education, and clinical status. E) Cross-sectional mediation analyses with centiloid as predictor, sTREM2 as mediator, and p-tau181 as dependent variable. F) Longitudinal mediation analyses with centiloid as predictor, sTREM2 as mediator, and change in p-tau181 as dependent variable. Early Aβ-accumulators are displayed in green, and late Aβ-accumulators in orange. Beta-estimates (B) and p-values for each path are displayed on the respective arrow. The average causal mediation effect [ACME] and the average direct effect [ADE] are displayed under each mediation triangle.

Data information: All models are controlled for age, sex, education, and clinical status.
sTREM2 is associated with amyloid-related p-tau increases and glucose hypermetabolism in Alzheimer's (2022)
Figure 2

Figure 2. Association between CSF sTREM2 and FDG-PET in early Aβ-accumulators (i.e. Aβ CSF+/PET−; n=70) and late Aβ-accumulators (i.e. Aβ CSF+/PET+; n=201). A) Plot shows significant (p<0.05) sTREM2 by group interaction on FDG-PET z-scores within an FDG-PET meta-ROI (Landau & Jagust, 2011) using a linear regression. B) T-value projection of the association between sTREM2 on FDG-PET, stratified by group. FDG-PET z-scores were derived by referencing FDG-PET SUVRs to cognitively normal controls (i.e. n=131; Aβ CSF−/PET−).

Data information: The models are controlled for age, sex, education, and clinical status. Boxplots are displayed as median (center line) ± inter-quartile range (box boundaries) with whiskers including observations falling within the 1.5 interquartile range. 200 Regions of interest are displayed per group.
Identification and function of conformational dynamics in the multidomain GTPase dynamin (2015)
Figure 3

Figure 3: Large conformational changes of the PHD identified by FRET.

(A) Design of a functional dynamin mutant to probe PHD stalk interactions. Minimal structure of the PHD and the PHD-Stalk interface showing the location of important residues discussed in this study. The unresolved loop L1NS in the stalk hosts the IAEDANS label and is sensitive to the two tryptophans (W525 and W542) in the PHD. The distance between two introduced cysteines (S357C and native C602) used to construct a double cysteine Dyn1 is also shown. (B) Comparison of emission spectra of various IAEDANS-labeled Dyn1 RCL variants (D352C, Y354C, S357C, I365C, H367C), upon Trp excitation at 295 nm. (C) FRET transfer upon excitation is contributed by two neighboring Trps (W525 and W542); Substitution by Phe resulted in significant loss of FRET. (D) IAEDANS emission kinetics upon addition of lipid nanotubes with or without PI4,5P2 (ex=295). The arrow indicates addition of lipids.
Identification and function of conformational dynamics in the multidomain GTPase dynamin (2015)
Figure 4

Figure 4: Biochemical properties of PHD ‘closed’ and ‘open’ states.

(A) Design of dynamin mutants to restrict the PHD in the closed (Dyn1Closed) or open (Dyn1ΔΔ) state. (B) Histogram shows basal and assembly-stimulated GTPase activities of non-crosslinked Dyn1CC vs crosslinked Dyn1Closed and Dyn1WT. Inset shows crosslinking of the PHD and stalk domains in Dyn1Y354C/S607C (Dyn1CC) with the bifunctional crosslinker, MTS-2-MTS, to yield Dyn1Closed, which migrates more slowly on SDS-PAGE, as well as liposome binding of Dyn1CC compared to Dyn1Closed (Bound, B; Unbound, UB). (C) Ability of Dyn1WT, Dyn1CC and Dyn1Closed to catalyze membrane fission and vesicle release from SUPER templates. (D) Size exclusion chromatographic profiles of Dyn1CC, Dyn1Closed at room temperature or after incubation for 10 min at 37°C. (E) Oligomeric state of Dyn1ΔΔ at room temperature. (F) Negative-stain electron micrographs of Dyn1WT, Dyn1ΔΔ and Dyn1Closed assembled onto lipid nanotubes. Scale bar = 200 nm (G) Curvature dependent liposome-stimulated GTPase activity of Dyn1WT and Dyn1ΔΔ. (H) Ability of Dyn1WT and Dyn1ΔΔ to catalyze membrane fission and vesicle release from SUPER templates.
Identification and function of conformational dynamics in the multidomain GTPase dynamin (2015)
Figure 5

Figure 5: Biochemical properties and PHD conformational dynamics of Dyn2, disease-associated S619L mutant

(A) Temperature dependence of basal and lipid stimulated GTPase activity of Dyn1WT and Dyn2S619L. (B) Temperature sensitive membrane fission activity of Dyn1WT, Dyn2WT and Dyn2S619L measured using SUPER templates. (C) Detection of Dyn2 PHD-stalk interactions by FRET using IAEDANS-labeled Dyn2L354C. (D) Curvature dependent membrane binding and consequent opening of PHD in Dyn1Y354C-IAEDANS and Dyn2L354C-IAEDANS. (E) Differential temperature dependence of PHD-stalk FRET for WT and S619L mutant Dyn2IAEDANS. Data are presented as relative FRET distances assuming a single donor/acceptor pair. (F) Differential solvent exchange kinetics of Dyn1S619L at ambient temperature compared to Dyn1WT under identical conditions. Yellow coloring indicates a significant increase in HDX. Quantitative data on the individual peptides used to generate this map are provided in (Appendix Fig. S5).
Identification and function of conformational dynamics in the multidomain GTPase dynamin (2015)
Figure 6

Figure 6: In vivo function of CNM-causing Dyn2 mutant S619L

(A,B) Transferrin receptor (TfnR) uptake, a measure of CME, shown as % uptake of total steady-state surface TfnR for control H1299 cells, and H1299 cells stabily expressing low amounts of siRNA-resistant Dyn2WT-EGFP (A) or Dyn2S619L-EGFP (B) with or without treatment of siRNA-directed towards endogenous Dyn2. (C) Fixed cell TIRF-M images of Dyn2WT-EGFP or Dyn2S619L-EGFP expressing H1299 cells with or without Dyn2-siRNA treatment showing co-localization with clathrin light chain immunostained rabbit anti-CLC and Alexa 547-conjugated secondary antibodies. (D) Percentage of Dyn2-EGFP positive clathrin coated pits detected by live cell TIRF-M and automated master/slave image analysis (Aguet et al, 2013). (E) Lifetime analysis of CCPs which are positive for EGFP-Dyn2WT or EGFP-Dyn2S619L with or without siRNA-mediated specific knockdown of endogenous Dyn2.
GENETICALLY-MODIFIED MACROPHAGES ACCELERATE MYELIN REPAIR (2022)
Figure 1

Figure 1. Graft-derived macrophages in demyelinating lesions

A. Bone marrow isolated from actin-GFP mice was transplanted into pre-conditioned recipients.

B. Flow cytometry analyses of recipient blood 2 months post-transplant. Bi. Transplanted cells detected by GFP fluorescence. Bii. CD11b lebelling shows a large proportion of monocytes expressing GFP.

C. Demyelinating lesions in chimeric mice at 3 dpl. Ci. Demyelination was induced by injecting LPC in the spinal cord white matter. Cii-Civ. Co-immunolabeling for GFP, MBP, and a mixture of CD11b/CD68, showing graft-derived macrophages in the lesion (identified by lack of MBP staining). White lines indicate lesion borders. Scale bar 20 µm. MBP-myelin basic protein; GFP-green fluorescent protein.
GENETICALLY-MODIFIED MACROPHAGES ACCELERATE MYELIN REPAIR (2022)
Figure 2

Figure 2. Genetically engineered HSCs secrete Sema3F that attracts OPCs in vitro.

A-C. Transduction of HSCs. A. Mouse bone marrow was isolated and differentiated cells (Lin+) were removed using MACS. Non-differentiated cells were transduced and expanded for 5 days. B. Lower numbers of GFP+ cells, verified using flow cytometry, after transduction with Sema3F vector, ***p<0.0001, Student t test, n=8 independent experiments. Mean±SEM. C. Western blot showing GFP expression in cells transduced with both vectors and Sema3F expression in the supernatant of Sema3F-transduced cells only.

D. OPCs isolated from adult PDGFRα-GFP mice using FACS were subjected to transwell-chamber migration assay in response to supernatants from non-transduced (NT), GFP-transduced (gfp), or Sema3F -transduced (sema3F-gfp) HSCs.

E. Fold increase in cells that crossed the membrane insert compared to NT. ***p‹0.0001. One-way ANOVA followed by Bonferroni's Multiple Comparison test. n= 1-2 normalized replicates from 3-5 independent experiments. Mean±SEM. ***p<0.0001. R.=recombinant. Super=supernatant. Anti-Nrp2=Neuropilin2 function blocking antibody.
GENETICALLY-MODIFIED MACROPHAGES ACCELERATE MYELIN REPAIR (2022)
Figure 3

Figure 3. Middle-age OPCs maintain Nrp2 expression and responsiveness to Sema3F.

A-B. Expression of Nrp2 gene by OPCs is maintained in middle-age (12 month (m) old) mice. A. Microarray analyses results for Nrp2 expression by OPCs purified using FACS from the brains of 2 months versus 12 months old PDGFRα−GFP mice (n=3-4 independent experiments). B. RNA sequencing results for Nrp2 expression by oligodendroglia-enriched preparations isolated from the spinal cords of 2 month versus 12 month old mice. (n=3-4 independent experiments). Mean±SEM

C-G. Sema 3F expression in demyelinating lesions at 4 dpl (onset of OPC recruitment) is decreased in middle-aged (12 m old) and old (18m old) mice compared to young mice (2m old). C-E. Colabellings for Sema3F and Iba1 (macrophage marker) in demyelinating lesions at 4 dpl in 2m (C), 12m (D),and 18m old mice (E). Arrowheads point to double-labelled cells. F. Quantification of Sema3F expressing cells in the lesion. G. Percentage of Iba1+ cells positive for Sema3F. NWM-normal white matter. dpl-days post lesion. n=4-8 mice/group. Mean±SEM Two-way ANOVA followed by Tukey's Multiple Comparison test. *p<0.05, **p<0.01, ***p<0.0001.

H. Transwell chamber assay was used to evaluate migration of young versus middle-age OPCs in response to recombinant Sema3F and supernatant from PGK-GFP-T2A-Sema3F transduced cells. OPCs of both ages migrate in response to recombinant Sema3F and PGK-GFP-T2A-Sema3F-transduced cell supernatant. n= 1-2 normalized replicates from 2-5 independent experiments. Mean±SEM. One-way ANOVA followed by Bonferroni's Multiple Comparison test. *p<0.05, ** p<0.01. Scale bar 50 µm.
GENETICALLY-MODIFIED MACROPHAGES ACCELERATE MYELIN REPAIR (2022)
Figure 4

Figure 4. Generation of Sema3F chimeras.

A. Transduced female HSCs were injected retro-orbitally into pre-conditioned male mice. Blood was analyzed 2 months post-transplant.

B. Percentage of transplanted (female) cells in the blood. n=18-19 mice/group. Mean±SEM

C. Percentage of transduced (GFP+) cells in the blood . Mean±SEM. ***p<0.0001. n=22-25 mice/group.

D. Percentages of GFP+ cells labeled with CD11b, CD19, and CD3. The proportion of GFP+ cells labeled with CD11b is increased in Sema3F mice (p=0.01), while that of CD19-labeled cells is decreased (p=0.0003). Mean±SEM. Unpaired Student t-test. n=9 mice/group. *p<0.05,***p<0.001.

E. Percentages of total blood cells expressing CD11b, CD19, and CD3. Red dashed lines indicate the percentage expression of these antigens in blood cells of control mice. n=9 mice/group. Mean±SEM.
GENETICALLY-MODIFIED MACROPHAGES ACCELERATE MYELIN REPAIR (2022)
Figure 5

Figure 5. Transgene-carrying macrophages in demyelinating lesions.

A-F. Co-labeling for GFP and MBP on spinal cord sections of GFP (A-C) and Sema3F-GFP chimeras (D-F) sacrificed at 7 (A,D), 10 (B,E), and 60 (C,F) days post lesion (dpl). Absence of MBP labeling in A-B,D-E indicates the lesion (delimited by yellow lines). Areas faintly labeled with MBP in C-F likely represent remyelinated areas.

G. Quantification of GFP+ cells. Kruskal-Wallis test p=0.02. No significant differences between GFP and Sema3F at any of the time points (Dunn's post test; Mann-Whitney test). Decrease in GFP+ cells between 7 and 60 dpl for both GFP and Sema3F mice 2m.

H-M. Co-labeling for GFP/MBP/Iba1 (macrophage/microglia marker) shows colocalization of GFP with Iba1. Arrows indicate double-labeled cells.

N-P Co-labeling for GFP and T cell marker CD3. Arrows indicate CD3-labeled cells.

Q-S. Co-labeling for GFP and B cell marker CD45R/B220. Arrows indicate CD45R/B220-labeled cells.

T. Percentages of GFP+ cells that are Iba1+, CD3+, and CD45R/B220+. The absolute majority of GFP+ cells are Iba1+.

U. Quantification of Iba1+, CD3+, and B220+ cells. For all 3 populations, no significant differences in cell numbers were observed between GFP and Sema3F mice, and a general decrease was observed at 60 dpl compared to earlier time points.

V-Aa. Co-labeling for GFP and microglial marker P2Y12. Purple arrows indicate P2Y12+ cells. Exclusion between the two markers is obvious in both groups.

Ab. Quantification of P2Y12+ cells. No significant changes are observed between the groups or across the time.

Data information: For all figure panels, n=6-7 mice/group for 7 and 10 dpl, n=2-3 mice/group for 60 dpl. Mean±SEM. Scale bars 20 μm, except for S (10 μm).
GENETICALLY-MODIFIED MACROPHAGES ACCELERATE MYELIN REPAIR (2022)
Figure 6

Figure 6. OPC recruitment is increased in Sema3F chimeras.

A. Temporal sequence of events in LPC lesion. dpl-days post lesion. Red inverted triangles indicate sacrifice.

B-G. Lesions at 7 dpl in GFP (B,E) and Sema3F (C,F) mice. B-C. Co-labeling for PDGFRα, MBP, and DAPI. Arrows indicate OPCs in the lesion. Bi and Ci-insets of white dotted squares in B and C. D. Higher numbers of PDGFRα+ (OPCs) cells in Sema3F mice at 7 dpl (Mann Whitney test: p=0.0031, n=6-8 mice/group). E-F. Co-labeling for Olig2 and MBP. E'-F'. Co-labeling for Olig2 and GFP of the lesions shown in E-F. 3D reconstructions. Proximity of OPCs and Sema 3F-carrying cells. E'i-E'iii and F'i-F'iii-insets of E'-F'. G. Higher numbers of Olig2+ (oligodendroglial) cells in Sema3F-GFP mice at 7 dpl (Mann Whitney test: p=0.0047, n=5-8 mice/group). ** p<0.01.

H-I. Immunolabelling for activated OPC marker Nkx2.2.

J. Numbers of Nkx2.2+ cells are increased in lesions of Sema3F-GFP mice at 7dpl (Mann Whitney test: p=0.014, n=6-7 mice/group). Arrows indicate Nkx2.2+ cells in close proximity of GFP+ cells. Mean±SEM. *p<0.05.

K-P. colabelling for Nkx2.2 and proliferation marker Ki67. Arrows indicate double labeled cells. Q. Numbers of Nkx2.2+Ki67+ cells are increased at 7 dpl in Sema3F-GFP mice. Mean±SEM. n=6-7 mice/group.

R. The proportion of Nkx2.2+ cells co-expressing Ki67 is unchanged. Mean±SEM. n=6-7 mice/group.

S-X. Colabelling for Olig2 and cleaved caspase 3, marker of apoptosis indicates occasional apoptotic cells in both groups of mice that are Olig2-. Arrows indicate cleaved caspase 3+ cells.Y. Numbers of cleaved caspase 3+ cells are the same in two groups. Mean±SEM. n=6 mice/group.

Data information: Scale bars 20 μm (B,C,E,F), 10 μm (H,I,M,P,U,X), 5 μm (Bi, Ci).
GENETICALLY-MODIFIED MACROPHAGES ACCELERATE MYELIN REPAIR (2022)
Figure 7

Figure 7. Oligodendrogenesis and remyelination are accelerated in Sema 3F chimeras.

A-B. Labelling for APC/CC1, a marker of oligodendrocytes. Dotted lines indicate the lesion border. APC+ cells are scarce in the lesions of GFP mice (A). B. APC+ cells in the lesion of Sema3F mice.

C. Quantification of APC+ cells (Mann Whitney test; p=0.0061 for 7 dpl, p=0.0081 for 10 dpl; n= 6-7 mice/group). *p<0.01.

D-E. EM images of the lesion in GFP (D) and Sema3F (E) chimeras at 14 dpl. Thin myelin sheaths in Sema 3F mice (yellow arrows).

F. Higher power image of a new myelin sheath in a Sema3F mouse. Fi. Inset of yellow square in F.

G. Quantification of remyelinated axons (Mann Whitney test: p=0.03, n=6 mice/group). *p<0.05.

H. In Sema3F mice, oligodendroglial cells (O) and early remyelination (*) are frequently observed in macrophage (M) vicinity. Hi. Inset of yellow dashed square in H.

Data information: Scale bars 20 μm (A,B), 1 μm (D,E), 500 nm (F).
NLRC3 expression in dendritic cells attenuates CD4+ T cell response and autoimmunity (2019)
Figure 1

Figure 1. NLRC3 deficiency promoted antigen-presenting function of DCs.

A. Representative flow cytometry data showing surface phenotypes of DCs sorted from spleens of wild type (WT) or Nlrc3-/- mice and treated with LPS (100 ng/ml) for 48 hours.

B. ELISA of cytokines in culture supernatants of DCs treated as in A.

C-F. The intracellular production of IFN-γ and IL-17 by CD4+ T cells (C), cytokines in culture supernatants (D), thymidine incorporation proliferation assay (E) and CFSE proliferation assay (F) among naive 2D2 CD4+ T cells stimulated with MOG(35-55) plus DCs treated as in A.

Data information: Data (n=5 in B, D and E) shown are the mean ±SD. **P < 0.01 and ***P < 0.001 by an unpaired t-test. Data are representative of three independent experiments with similar results.
NLRC3 expression in dendritic cells attenuates CD4+ T cell response and autoimmunity (2019)
Figure 2

Figure 2. NLRC3 deficiency promoted EAE development.

WT and Nlrc3-/- mice were immunized with MOG(35-55) peptide in CFA adjuvant and pertussis toxin to induce EAE.

A. Mean clinical scores of EAE in immunized WT (n= 10) and Nlrc3-/- mice (n= 10).

B. Representative flow cytometry data showing intracellular production of IFN-γ and IL-17A by CD4+ T cells from the spinal cord and brain of WT or Nlrc3-/- mice 26 d after EAE induction after restimulation with MOG(35-55) peptide. Pooled data are presented in the right panel.

C. Representative flow cytometry data showing surface phenotypes of DCs from spleens of WT or Nlrc3-/- mice 26 d after EAE induction.

D. Expression of Nlrc3, Il12, Il6, Il23 and Il27 mRNA in DCs sorted from WT and Nlrc3-/- mice 26 d after EAE induction, presented relative to that of Gapdh.

Data information: Data (n=5 in B right and D) shown are the mean ±SD. *P < 0.05, **P < 0.01and ***P < 0.001 by an unpaired t-test. Data are representative of three independent experiments with similar results.