EMBO/sd-character-level-ner huggingface dataset:
Figure 1(A) Mice were orally administered with Mulberry bark derived exosome-like nanoparticles (MBELNs) (10 x 109 particles/100 µl/mouse) or phosphate buffered saline (PBS) for seven days. Heat map showing influence of MBELNs on colonic gene expression from three biological replicates. (B) In vitro assessment of MBELN-dependent induction of aryl hydrocarbon receptor (AhR) promoter using HEPA1.1 cells (contain AhR responsive luciferase reporter construct). Data are mean ± SEM from three biological replicates. **P<0.01, ***P<0.001 using one-way ANOVA. (C) Representative images showing expression of pAhR in MC38 cells and Caco2 cells treated with MBELNs from three biological replicates. Scale bar 20 μm. (D) Western blot (top) and graphical representation of fold changes (bottom) for AhR in MC38 cells, Caco2 cells and colon epithelial cells after treatment with MBELNs. Data are mean ± SEM of three biological replicates. *P<0.05 using Student's t-test. (E) Fecal microbiota were analysed following administration of MBELNs (10 x 109 particle/100 µl/dose/day/mouse) for 7 days to C57BL/6 mice. Alpha diversity (Shannon index) was calculated at the family level and is displayed as a bar-and-whiskers plot for each individual combination of control and MBELN treatment. The centre line represents the median and the box encloses the 1st and 3rd quartiles ("hinges"). The upper and lower whiskers represent the furthermost points from the respective hinges, which are no more than 1.5 interquartile ranges from the hinge. The individual points are overlaid. Data are presented from five mice or biological replicates. (F) Beta diversity analysis, biplots- samples (points) and bacterial taxa at family level (axes) are simultaneously projected on the two-dimensional canonical axes (CA1 and CA2). Data are presented from five mice or biological replicates. (G) Pictorial representation of Dextran sulfate sodium (DSS; 2%) induced colitis development in mice. (H) Graph showing loss of weight following DSS-induced colitis with and without MBELN treatment. Data are mean ± SEM of seven biological replicates, **P<0.01 using Mann-Whitney test. (I) Representative image showing changes in colon morphology and length following DSS-induced colitis with concurrent treatment with MBELNs. (J) Column graph showing changes in colon length. Data are mean ± SEM from seven biological replicates, **P<0.01 using one-way ANOVA. ( Hematoxylin and eosin (HE) staining to show histological changes in colon tissue Scale bar 200 μm. a graph showing severity score (right) based on histological data. Data are mean ± SEM of seven biological replicates, **P<0.01 using Student's t-test. (M) Enzyme-linked immunosorbent assay (ELISA) for interleukin (IL)-6 and IL-1β from colon tissue. Data are mean ± SEM from seven biological replicates, **P<0.01 using one-way ANOVA.
JQ1 treatment inhibits microglial expression of inflammatory cytokines in the rd10 retina.Fig. 4 JQ1 treatment inhibits microglial expression of inflammatory cytokines in the rd10 retina. Intravitreal injection of JQ1 (or vehicle) was performed at PN14, as described in Fig. 1. Retinas were collected at PN24. a Homogenates were prepared from retinas (3 groups, total 12 mice) and used for qRT-PCR. Quantification: normalization to GAPDH mRNA; mean ± SEM; n = 3 independent homogenation/qRT-PCR experiments; *P < 0.05, **P < 0.01 compared to rd10 vehicle control. b Retinal homogenates were used for determination of MCP-1 protein levels by ELISA. Quantification: normalization to WT mice injected with vehicle; mean ± SEM; n = 3 experiments; *P < 0.05. c Retinal microglia were purified from dissociated rd10 retinas via flow sorting, as described in 'Methods'. Sorting was performed five times using retinas collected from five groups of rd10 mice (four mice each). Sorted microglial cells (CD11b + CD45low) were then subjected to qRT-PCR. Quantification: normalization to GAPDH mRNA; mean ± SEM; n = 5; *P < 0.05, **P < 0.01, compared to rd10 vehicle control. d Microglial cells were isolated and purified from B6 mouse brains. Cells were pre-incubated with vehicle (DMSO) or JQ1 (0.5 μM) for 12 h, and then induced for inflammatory cytokine expression with LPS (1 μg/ml) for another 2 h prior to qRT-PCR assay. Quantification: normalization to GAPDH mRNA; mean ± SEM; n = 3 independent experiments; *P < 0.05, **P < 0.01 compared to vehicle + LPS
Figure 5(A) The effect of indicated mutations on H2A.Z deposition as determined by immunoblotting. Chromatin-associated proteins were extracted and subjected to immunoblotting by the anti-H2A.Z antibody. The histone H4 level was detected by the anti-H4 antibody and indicated as a loading control. (B) Meta plots showing H2A.Z occupancy on H2A.Z target genes. TSS, transcription start site; TTS, transcription termination site. RPKM, reads per kilobase per million. The H2A.Z ChIP-seq results were generated from two independent biological replicates. (C) Venn diagrams showing overlaps of genes with lower H2A.Z levels in the pie1, mbd9-1, and chr11/17 mutant than in the WT. The significance of the overlaps between each pair of samples was determined by hypergeometric test (P0).  (D) Heat maps showing H2A.Z enrichment in the WT, pie1, chr11/17, and mbd9-1 mutants over the PIE1-dependent H2A.Z target genes. The peaks were sorted by H2A.Z density in the WT. (E) Shown are H2A.Z changes in the pie1, chr11/17, and mbd9-1 mutants relative to the WT. PIE1-dependent H2A.Z target genes were subjected to the analysis and sorted by H2A.Z density in the WT. The color bar shows log2(fold change). (F) Meta plots showing CHR11 and PIE1 occupancy on PIE1-dependent H2A.Z target genes. TSS, transcription start site; TTS, transcription termination site. The CHR11-Flag and PIE1-Flag ChIP-seq data are from two independent biological replicates. (G) Heat maps showing the enrichment of PIE1-Flag and CHR11-Flag over the PIE1-dependent H2A.Z target genes. The peaks were sorted by H2A.Z density in the WT. (H) Box plot showing the enrichment of CHR11 and PIE1 over H2A.Z target genes and non-H2A.Z target genes. The log2(fold change) values of RPKM between the CHR11-Flag or PIE1-Flag signals and the WT signals are shown. Center lines and box edges represent medians and the interquartile range (IQR), respectively. Whiskers extend to minimum and maximum values within 1.5 times of the IQR. The data shown are from two independent biological replicates. The difference between the CHR11-Flag and PIE1-Flag ChIP-seq levels was determined by student's t test. ** P<0.01.
Gid4 and Gid10 compete for binding to GIDAnt Lysates from wildtype, ∆Gid4, and Gid4∆C strains expressing endogenously tagged 3xFLAG-Gid10 that were grown at 42°C for one hour, and then returned to 30°C for the indicated timepoints were run on an SDS-PAGE gel and immunoblotted with αFLAG and αPGK.Figure 2Lysates from wildtype, ∆Gid4, and Gid4∆C strains expressing endogenously tagged 3xFLAG-Gid10 that were grown at 42°C for one hour, and then returned to 30°C for the indicated timepoints were run on an SDS-PAGE gel and immunoblotted with αFLAG and αPGK. Wildtype and Gid10 overexpressing yeast strains expressing endogenously tagged Gid4 were grown for 19 hours in YPE, and transitioned to YPD for the indicated timepoints. Lysates were run on an SDS-PAGE gel and immunoblotted with αFLAG and αPGK. Points represent mean, error bars represent standard deviation (n>3 biological replicates). Fbp1 protein abundance in wildtype and Gid10 overexpressing yeast strains grown in ethanol medium (YPE) for 19 hours, and following 30 minutes and 2 hours glucose recovery. Bars represent mean, error bars represent standard deviation, significance was determined by one-way ANOVA (unpaired) followed by Tukey's multiple comparison test, * indicates p<0.05, ** indicates p<0.01, (n=3 biological replicates). In vitro competition assay probing the ability of N-terminally 2xStrep-tagged Gid4 (2xS-Gid4) to exchange with Gid10 in the GIDSR10 complex. Proteins after Strep-Tactin pull-down were visualized by Coomassie-stained SDS-PAGE.
Figure 1(A) Coordinates for injection in normal NHPs of the pilot group, study group 1 and study group 2 were calculated on the bases of pre-surgery MRI scans. (B) 3D rendering of injected brains generated based on post-surgery MRI scans showing the injection sites and the brain volume containing the vector suspension in the different treatments groups. EC, External capsule; Thal, thalamus; CR, corona radiata; ant, anterior; post, posterior. (C) The brain was cut in 6 mm-thick slices using an adjustable brain matrix, obtaining 9-10 slices/brain. (D) Each brain slice was divided along the midline and each part subdivided in blocks. The cervical spinal cord was cut in 4 blocks.
Figure 2(A) Immunoblotting of NSC34 cells expressing AR-24Q or AR-97Q (NSC24Q and NSC97Q, respectively) that were treated with DHT for Dnmt1, Dnmt3a and Dnmt3b, and quantification of the signal intensities of bands corresponding to Dnmt1, Dnmt3a and Dnmt3b (n = 3). (B) Relative mRNA levels of Dnmt1 in NSC24Q and NSC97Q cells measured with RT-qPCR (n = 3). (C) Protein levels of Dnmt1, Dnmt3a and Dnmt3b in DHT-treated and -untreated NSC97Q cells by Western blotting analysis. (D) RT-qPCR analysis of Dnmt1 in DHT-treated and -untreated NSC97Q cells (n = 3). (E, F) Quantitative assessment of cell viability changes due to the siRNA-mediated knock down of Dnmt1, Dnmt3a or Dnmt3b in NSC97Q cells with DHT (E) or without DHT (F) using the WST-8 assay (n = 3). (G) Quantitative assessment of the cell viability of NSC97Q cells treated with DHT and RG108 using the WST-8 assay (n = 3 per group). (H) Immunoblotting of NSC97Q cells treated with DHT and RG108 for Dnmt1, Dnmt3a and Dnmt3b. (I, J) Cell viability analysis with siRNA-mediated knockdown of Dnmts in DHT-untreated NSC97Q (I) and DHT-treated NSC24Q (J).
Figure 3(A) Barrier integrity was analysed by TEER measurements of Caco-2 and Calu-3 over a period of 20 days (n=3 donors measured in quadruplicates). TEER: Transepithelial electrical resistance. (B) ACE2 cell surface expression on Caco-2 and Calu-3 was determined by quantitative real-time PCR. Data information: Data show the mean values and error bars are the SEM. Statistical analysis was performed using ordinary one-way ANOVA with Tukey's multiple-comparison test. *P≤0.05, **P≤0.01 (n=5 Caco-2 donors measured in monoplo), *p=0.0460 (n=5 Calu-3 donors measured in monoplo) (C, D) SARS-CoV-2 binding was measured in polarized Caco-2 (C) and Calu-3 (D) cells in presence or absence of antibodies against ACE2 (cell incubation), and UF heparin (250 IU/mL) or LMWH enoxaparin (250 IU/mL) (virus incubation). Data information: Data show the mean values and error bars are the SEM. Statistical analysis was performed using ordinary one-way ANOVA with Tukey's multiple-comparison test. *P≤0.05, **P≤0.01, ***P≤0.001, ****P≤0.0001 (C) (n=3 Caco-2 donors measured in triplicate), (D)(n=3 Calu-3 donors measured in triplicate) (E) Polarized Calu-3 were inoculated with 0.5 TCID/mL of a SARS-CoV-2 isolate (hCoV-19/Italy) either directly or in presence of antibodies against ACE2 or upon pre-treatment with LMWH enoxaparin (250 IU/mL) for 30 min at 37°C. Virus was detected by lysing after 48 hours through quantitative real-time PCR of viral RNA (E) and virus production was determined by detection of viral RNA in supernatant using quantitative real-time PCR (F). Data information: Data show the mean values and error bars are the SEM. Statistical analysis was performed using (E, F) ordinary one-way ANOVA with Tukey's multiple-comparison test. *P≤0.05, **P≤0.01, ***P≤0.001, ****P≤0.0001 (n=3 donors measured in monoplo). TEER: Transepithelial electrical resistance.
a) HEK293 cells were co-transfected with vectors encoding ULK1–HA and ULK1–Myc and then grown either in normal (Ctrl) or in starvation (EBS) medium for 1 h.figf6(a) HEK293 cells were co-transfected with vectors encoding ULK1-HA and ULK1-Myc and then grown either in normal (Ctrl) or in starvation (EBS) medium for 1 h. Protein extracts were immunoprecipitated using an anti-Myc antibody, and analysed by western blotting using anti-HA, and anti-Myc antibodies. Quantification is shown on the right. n = 3 extracts prepared from independent experiments. Data are presented as means±s.d. and significance is P = 0.001. (b) HEK293 cells were transfected with TRAF6 RNAi oligonucleotide (TRAF6 siRNA) or unrelated oligonucleotides as a control (Ctrl siRNA). Then, cells were co-transfected with vectors encoding ULK1-HA and ULK1-Myc and protein complexes were immunoprecipitated using anti-Myc antibody. Protein extracts were analysed by western blotting using anti-HA, anti-Myc and anti-TRAF6 antibodies. Quantification of ULK1-HA relative to ULK1-Myc is reported on the right. n = 3 extracts prepared from independent experiments. Data are presented as means±s.d. and significance is P = 0.037. (c) HEK293 cells were transfected with AMBRA1 RNAi oligonucleotide (AMBRA1 siRNA) or unrelated oligonucleotides as a control (Ctrl siRNA). Then, cells were co-transfected and analysed as in a. Quantification is shown on the right. n = 3 extracts prepared from independent experiments. Data are presented as means±s.d. and significance is P = 0.044. (d) HEK293 cells were co-transfected with vectors encoding for ULK1-HA, ULK1-Myc and AMBRA1WT or AMBRA1AA respectively. Protein complexes were immunoprecipitated and analysed as in a. Quantification is shown on the right. n = 3 extracts prepared from independent experiments. Data are presented as means±s.d. and significance is P = 0.014.
Figure 3A HDX-MS reveals a significant increase in deuteration at positions E24 (α1) and R169 (α7) following activation with cBID. These positions are conserved suggesting a potentially important hydrogen bonding interaction. B BAK, or BAK with cysteine introduced at the indicated positions (on a BAK∆Cys background) were stably expressed in Bax-/-Bak-/- MEFs and assess for BAK expression by immunoblotting (inset panel; * indicates non-specific band.) and apoptotic activity in response to etoposide treatment. C E24 and R169 are proximal in inactive BAK on mitochondria. Mitochondria-enriched membrane fractions from cells were incubated with oxidant (CuPhe) and induced intramolecular disulphide linkage of BAK was assessed on non-reducing SDS-PAGE. D E24 and R169 dissociate during BAK activation. Mitochondria-enriched membrane fractions from cells were incubated with cBID (100 nM) prior to oxidant (CuPhe) and the induced intramolecular and intermolecular disulphide linkage of BAK was assessed on non-reducing SDS-PAGE.
Figure 1(A) Flow cytometry analysis of CD34+CD1a- thymocytes cultured in FTOCs, in the presence of a control or anti-Notch1 blocking antibody. Numbers in dot plots indicate percentage of cells for the corresponding populations. Histograms show TCRγδ expression in CD3+TCRαβ+ (blue) and CD3+TCRαβ- (red) cells.(D) Flow cytometry analysis of CD34+CD1a- thymocytes submitted to FTOC with fetal thymic lobes deficient for Dll4 and/or Jag2 (Cre+) as indicated above the dot plots. Numbers in dot plots indicate percentage of cells for the corresponding populations. Histograms show TCRγδ expression in CD3+TCRαβ+ (blue) and CD3+TCRαβ- (red) cells.
Loss of Dcp-1 promotes mitochondrial elongation.Figure 5.(A) l(2) mbn cells were labeled with the ATPsyn-α, and mitochondrial morphology was scored as fragmented, normal, or elongated. (B) Cells were treated with control or Dcp-1 dsRNA and subjected to nutrient-rich media or 1 h of starvation. Quantifications represent the percentage of cells with elongated mitochondria divided by the total number of cells examined. At least 100 cells were examined manually in three independent experiments (n = 3). Error bars represent the mean ± SD. Statistical significance was determined using one-way ANOVA with a Bonferroni post test (*, P < 0.05; **, P < 0.01). (C) Mitochondrial targeted GFP (mitoGFP) was expressed in the germline using the nosGAL4 driver. Staining shows mitoGFP, Armadillo, and DNA. (D) Mitochondria were scored as healthy (H), clustered (C), or elongated and overly connected (E). All of mitochondria from fed UASp-mitoGFP/+;nosGAL4/+ flies were scored as healthy. n = 15 egg chambers manually scored. (E) mitoGFP was expressed in Dcp-1Prev1 flies using the nosGAL4 driver. (F) 54% of egg chambers from UASp-mitoGFP/+;Dcp-1Prev1/Dcp-1Prev1;nosGAL4/+ flies contained elongated mitochondria, 39% contained mitochondria that were scored as healthy, and 7% contained clustered mitochondria. n = 28 egg chambers manually scored.
Figure 6A) Heat map showing recovery of ZNFX-1 fluorescence after photobleaching in Z granules from pachytene stage adult germ cells from wild-type or zsp-1(gg682) mutant animals. Scale bar, 0.5 μm. B) Normalized recovery of fluorescence after photobleaching of GFP::ZNFX-1 in wild-type or zsp-1(-) mutant animals over indicated time points. Bleaching event occurred at 0s. Data are represented as ± s.e.m. of n=13, and n=16 individual granules from wild-type and zsp-1(gg682) animals, respectively.
Figure 4(A)-(C) The scattering profiles (A), the PDDFs (B) and the dimensionless Kratky plots (C) of xrRNA1-2s from DENV2 (cyan), ZIKV (red) and WNV (blue). The inset in (A) shows the guinier regions of the respective scattering profiles with linear fit lines. The dimensionless Kratky plot of ZIKV xrRNA1 (red dashed line) was included in (C) for comparison, indicating that the structures of xrRNA1-2s are all well folded. (D) The ab initio shape envelopes of the xrRNA1-2s of DENV2 (left), ZIKV (middle) and WNV (right). The atomic models from rigid-body modeling by Xplor-NIH are superimposed onto the respective envelopes. The back-calculated scattering profiles of the atomic models were fitted to the respective experimental scattering profiles in (A).
Figure 6(A) Gene expression pattern of BCL11B (red dots) and HES1 (blue squares) during human T cell development, derived from microarray data as shown in Figure 2. (n=2 biological replicates and error bars indicate SEM). Quantitative RT-PCR expression analysis of BCL11B in human after 5 days, respectively, of coculture on OP9 stromal cells expressing different Notch ligands. Graphs show mean expression, relative to the geometric mean of ACTIN and GAPDH and relative to the OP9-DLL1 cultured cells (n=4 independent experiments with different donors, error bars indicate SEM and * indicates p<0.05 and ns (not significant) indicates p>0.05 in a paired t-test). Quantitative RT-PCR expression analysis of BCL11B in human CD34+ thymocyte progenitors after 2 days, respectively, of coculture on OP9 stromal cells expressing different Notch ligands. Graphs show mean expression, relative to the geometric mean of ACTIN and GAPDH and relative to the OP9-DLL1 cultured cells (n=4 independent experiments with different donors, error bars indicate SEM and * indicates p<0.05 and ns (not significant) indicates p>0.05 in a paired t-test). (D) Quantitative RT-PCR expression analysis of BCL11B in human CD34+ thymocyte progenitors after 2 days of coculture on OP9-DLL1 stromal cells in the presence of 5 µM DAPT (GSI). Graphs show mean expression, relative to the geometric mean of ACTIN and GAPDH and relative to sample cultured in the presence of control DMSO (n=4 independent experiments with different donors, error bars indicate SEM and * indicates p<0.05 in a paired t-test). Quantitative RT-PCR expression analysis of miR-17 in human CB CD34+Lin- after 5 days, respectively, of coculture on OP9 stromal cells expressing different Notch ligands Graphs show mean expression, relative to the geometric mean of SNORD61, SNORD95 and RNU6-2 and relative to the OP9-DLL1 cultured cells (n=2 independent experiments with different donors; error bars indicate SEM - the two data points are shown). Quantitative RT-PCR expression analysis of miR-17 in human CD34+ thymocyte progenitors after 5 and 2 days, respectively, of coculture on OP9-DLL1 stromal cells in the presence of 5 µM DAPT (GSI). Graphs show mean expression, relative to the sample cultured in the presence of control DMSO (F) (n=2 independent experiments with different donors; error bars indicate SEM - the two data points are shown). (G) Quantitative RT-PCR gene expression analysis of BCL11B in control (black bar), GATA3 shRNA or TCF7 shRNA (grey bars) transduced CD34+ thymocytes after 48h of coculture on OP9-DLL1 stromal cells, relative to the geometric mean of ACTIN and GAPDH and relative to the control-transduced sample (n=6 independent experiments with different donors for GATA3 shRNA, n=4 independent experiments with different donors for TCF7 shRNA, error bars indicate SEM and * indicates p<0.05 in a paired t-test).
Figure 2(A) Larval NSCs of control (ctrl; yw) and pr-set7716/Df(3R) ED5644 (716/Df) at 0h, 24h and 48h ALH were stained for Pr-set7, Dpn and Mira. Yellow dotted boxes, zoomed-in area. Data information: White arrows point to NSCs. Scale bars 15 μm (A). (B) Quantifications of the corrected total cell fluorescence (CCF) for genotypes in (A). CCF = Integrated Density - (area of selected cell × mean fluorescence of background readings). At 0h ALH, CCFs were 735.7±220.7 (n=168) for control, 302.1±150.0 (n=160) for 716/Df. At 24h ALH, CCFs were 2238.3±628.4 (n=158) for control, 310.4±207.1 (n=113) for 716/Df. At 48h ALH, CCFs were 3834.0±924.2 (n=124) for control, 465.9±295.0 (n=126) for 716/Df. Data are presented as mean ± SD. Statistical analyses were done comparing between the CCFs at later time points with the CCFs for control at 0h ALH using Mann-Whitney test . ***P < 0.001. Data information: Quantification data are presented in as mean ± SD (B Statistical analyses were done comparing two different genotypes using Mann-Whitney test (B, ns: non-significant. (C) Larval NSCs of control (ctrl; yw), pr-set7716/Df, pr-set7716/Df with UAS-pr-set7 induced with insc-Gal4, and pr-set7716/Df with pr-set7-BAC at 24h ALH were stained for H4K20me1, Dpn, Mira and DAPI. Control: n=108; pr-set7716/Df: n=87; pr-set7716/Df with UAS-pr-set7 induced with insc-Gal4: n=167 and pr-set7716/Df with pr-set7-BAC: n=104. Data information: White arrows point to NSCs. Scale bars, 5 μm (D) A schematic representation of the FUCCI. (E) Larval NSCs with FUCCI constructs induced with insc-Gal4 at 24h were stained for GFP, RFP, Dpn, and Prospero (Pros). (F) Quantifications of quiescent NSCs in different cell-cycle stages from FUCCI flies (induced with insc-Gal4) in control (and insc-Gal4>FUCCI) and pr-set7716/Df. Quiescent NSCs of insc-Gal4>FUCCI: 76.1%±1.5% in G2, 1.7%±0.2% in S and 22.2%±1.3% in G0 (n=343). Quiescent NSCs of insc-Gal4>FUCCI; pr-set7716/Df: 74.4%±1.0% in G2, 0.9%±0.2% in S and 24.7%±0.8% in G0 (n=344). Data information: Quantification data are presented in as mean ± SD Statistical analyses were done comparing two different genotypes using Mann-Whitney test ns: non-significant. White arrows point to NSCs. Scale bars, 5 μm
a) Activation of the gB-specific CD8+ T cell hybridoma (which expresses β-galactosidase as an indicator of T cell activation) by macrophages infected for various times (horizontal axis) with HSV-1, then incubated for 12 h at 37 °C with the hybridoma.figf1(a) Activation of the gB-specific CD8+ T cell hybridoma (which expresses β-galactosidase as an indicator of T cell activation) by macrophages infected for various times (horizontal axis) with HSV-1, then incubated for 12 h at 37 °C with the hybridoma. A595, absorbance at 595 nm. b) Activation of the hybridoma as described in a, with the addition of dimethyl sulfoxide (DMSO; negative control), bafilomycin A (Baf), brefeldin A (BFA) or MG-132 at 2 h after macrophage infection. (c) Activation of the hybridoma as described in a, with the addition of bafilomycin A at 2 h after macrophage infection. (d) Immunofluorescence microscopy of gB (blue) and LAMP-1 (red) in HSV-1-infected macrophages; pink indicates colocalization. Original magnification, × 40. (e) CD8+ T cell-stimulatory capacity (as described in a) of uninfected macrophages (Mock), of BMA (BMA-HSV) or J774 (J774-HSV) macrophages infected for 8 h with HSV-1, and of cocultures of J774 macrophages (H-2d) infected for 1 h with HSV-1, then mixed with uninfected BMA (H-2b) macrophages at a ratio of 1:1 and cultured together for 8 h (J774-HSV + BMA).