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1.
FIG. 3.

FIG. 3. From: Lack of Intrinsic CTLA-4 Expression Has Minimal Effect on Regulation of Antiviral T-Cell Immunity .

TCR repertoire and functional avidities of virus-specific T cells. (A) CD4+ T-cell TCR repertoire. TCR Vβ usage by GP61-specific CTLA-4+/+ (black) and CTLA-4−/− (light gray), as well as other CTLA-4+/+ (black hatched) and CTLA-4−/− (gray hatched), CD4+ T cells is shown 8 days after LCMV infection. Arrows indicate narrowing (degeneration) of the TCR repertoire among GP61-specific T cells compared to other CD4+ T cells. (B) Functional avidities of virus-specific effector T cells. Effector T-cell populations were incubated with graded concentrations of MHC class I (GP33) or II (GP61) peptides and subsequently stained for intracellular IFN-γ. Functional avidities were measured as peptide concentrations that elicited detectable IFN-γ production in 50% of a specific T-cell population. The 50% effective concentration was 5.3 × 10−10 M for CTLA-4+/+ GP33-specific CD8+ T cells, 6.1 × 10−10 M for CTLA-4−/− GP33-specific CD8+ T cells, 6.0 × 10−8 M for CTLA-4+/+ GP61-specific CD4+ T cells, and 1.1 × 10−7 M for CTLA-4−/− GP61-specific CD4+ T cells. Closed symbols, CTLA-4+/+; open symbols, CTLA-4−/−.

Dirk Homann, et al. J Virol. 2006 January;80(1):270-280.
2.
FIG. 5.

FIG. 5. From: Lack of Intrinsic CTLA-4 Expression Has Minimal Effect on Regulation of Antiviral T-Cell Immunity .

Secondary T-cell responses in the absence of intrinsic CTLA-4 expression. Memory T cells obtained ∼8 months after primary infection of mixed CTLA-4 chimeras were transferred into congenic (CD45.1) hosts that were subsequently challenged with high-dose LCMV. (A) Epitope-specific CD8+ T-cell responses. GP33-specific CD8+ T-cell responses by donor CTLA-4+/+ (CD45.2+ Thy1.1+), donor CTLA-4−/− (CD45.2+ Thy1.1), and host CTLA-4+/+ (CD45.2 Thy1.2) CD8+ T cells 6 days after rechallenge are shown. (B) Quantitation of secondary T-cell responses. Absolute numbers of splenic epitope-specific CD8+ T cells identified by MHC class I tetramer staining are shown (black, CTLA-4+/+ donor; gray, CTLA-4−/− donor; white, CTLA-4+/+ host). (C) Extent and distribution of LCMV-specific secondary T-cell responses. Epitope-specific T cells identified 6 days after secondary challenge by intracellular cytokine staining are shown. CTLA-4+/+ donor, black bars; CTLA-4−/− donor, gray bars; CTLA-4+/+ host, white bars. Values represent the mean ± the standard error of the mean of four mice per group.

Dirk Homann, et al. J Virol. 2006 January;80(1):270-280.
3.
FIG. 6.

FIG. 6. From: Lack of Intrinsic CTLA-4 Expression Has Minimal Effect on Regulation of Antiviral T-Cell Immunity .

Effect of IDO blockade on primary virus-specific T-cell responses. B6 mice, as well as control and mixed CTLA-4 chimeras, were implanted with slow-release pellets containing the IDO inhibitor 1-methyl-tryptophan or placebo pellets. One day after implantation, mice were infected with LCMV and frequencies of specific T cells (GP33-specific CD8+ and GP61-specific CD4+ T cells) were determined 8 days later. (A) IDO blockade in B6 mice and control chimeras. The congenic CTLA-4+/+ Thy1.1+ and Thy1.2+ populations in control chimeras gave equivalent results and are therefore displayed with combined values. Statistically significant differences between CTLA-4+/+ and CTLA-4−/− T-cell populations were calculated by Student's t test (ns, not significant; *, P = 0.0292; **, P = 0.0083). (B) IDO blockade in mixed CTLA-4 chimeras indicates differential responsiveness in CTLA-4+/+ and CTLA-4−/− compartments. Values represent the mean ± the standard error of the mean of three mice per group in one of two independent experiments.

Dirk Homann, et al. J Virol. 2006 January;80(1):270-280.
4.
FIG. 4.

FIG. 4. From: Lack of Intrinsic CTLA-4 Expression Has Minimal Effect on Regulation of Antiviral T-Cell Immunity .

Survival and homeostatic proliferation of memory T cells. (A) Maintenance of T-cell memory. The extent and distribution of LCMV-specific T-cell memory were evaluated among CTLA-4+/+ (black bars) and CTLA-4−/− (gray bars) T cells 238 days after infection by intracellular cytokine staining. Representative data (mean ± the standard error of the mean) for two or three mice tested in two independent experiments are shown. (B) Determining proliferation by BrdU chase. After pulsing CD8+ and CD4+ T cells during the first 8 days of virus infection, mice were switched to regular drinking water and loss of BrdU by T cells was monitored. Approximately 8 months after infection, only a fraction of the CD8+ and CD4+ T cells retained detectable BrdU. Black bars, CTLA-4+/+; gray bars, CTLA-4−/−. (C) Proliferation of specific memory T cells. Expression of the nuclear cell proliferation-associated antigen Ki-67, expressed in all active stages of the cell cycle, is shown 238 days after virus infection in GP33-specific CD8+ (top) and GP61-specific CD4+ (bottom) T cells identified by intracellular IFN-γ staining. (D) Bcl-xL expression by virus-specific T cells. Bcl-xL (black tracings) was detected in GP33-specific CD8+ (top) and GP61-specific CD4+ (bottom) T cells identified by intracellular IFN-γ staining 238 days after virus infection as detailed in Materials and Methods. Gray histograms, isotype staining. Values indicate the normalized geometric mean of fluorescence intensity derived by dividing the geometric mean fluorescence intensity of Bcl-xL staining by the geometric mean fluorescence intensity of corresponding isotype control staining.

Dirk Homann, et al. J Virol. 2006 January;80(1):270-280.
5.
FIG. 1.

FIG. 1. From: Lack of Intrinsic CTLA-4 Expression Has Minimal Effect on Regulation of Antiviral T-Cell Immunity .

Phenotype and functional profile of T cells from mixed CTLA-4 bone marrow chimeras. (A) Activation and memory marker expression on CTLA-4+/+ and CTLA-4−/− T cells. Splenocytes from aged bone marrow chimeras (∼8 months after reconstitution) were stained for CD8 (top) or CD4 (bottom), as well as Thy1.1, CD44, and CD69. Dot plots are gated on CD8+ or CD4+ T cells among Thy1.1+ CTLA-4+/+ (left) or Thy1.1 CTLA-4−/− (right) populations. (B) Cytokine profiles of CTLA-4+/+ and CTLA-4−/− CD4+ T cells. Peripheral blood lymphocytes were polyclonally stimulated and stained for CD4 and the indicated cytokines as detailed in Materials and Methods. Percentages of cytokine-producing CD4+ T cells among CTLA-4+/+ (black bars) and CTLA-4−/− (gray bars) CD4+ T cells are shown. Values and error bars represent the standard error of the mean of four mice tested (n = 4 per group). (C) IFN-γ production and CTLA-4 expression by virus-specific CD4+ T cells. Eight days after LCMV infection, IFN-γ production and CTLA-4 expression by CTLA4+/+ and CTLA-4−/− CD4+ T cells were analyzed in the same sample (top right, gated on Thy1.1+ [CTLA-4+/+] cells; bottom right, gated on Thy1.1 [CTLA-4−/−] cells). CTLA-4−/− CD4+ T cells also serve as internal negative controls for CTLA-4 staining. (D) CTLA-4 expression levels in virus-specific CD4+ and CD8+ T cells. Values on the right (gated on virus-specific [IFN-γ+] CD4+ or CD8+ T cells) indicate the geometric mean fluorescence intensity of CTLA-4 staining among GP61-specific CD4+ (upper) and GP33-specific CD8+ (lower) T cells (black tracings, Thy1.1+ IFN-γ+ CTLA-4+/+ cells; gray histograms, Thy1.1 IFN-γ+ CTLA-4−/− cells).

Dirk Homann, et al. J Virol. 2006 January;80(1):270-280.
6.
FIG. 2.

FIG. 2. From: Lack of Intrinsic CTLA-4 Expression Has Minimal Effect on Regulation of Antiviral T-Cell Immunity .

Analysis of the primary T-cell response in mixed CTLA-4 bone marrow chimeras. (A) Antigen-driven proliferation. The extent of antigen-driven CD8+ and CD4+ T-cell proliferation during the first 8 days of virus infection was determined by BrdU incorporation as detailed in Materials and Methods. Black bars, CTLA-4+/+ cells; gray bars, CTLA-4−/− cells. (B) Magnitude and epitope distribution of the virus-specific T-cell response. The fraction of epitope-specific T cells was determined 8 days after LCMV infection by intracellular cytokine staining as detailed in Materials and Methods. Data (mean ± the standard error of the mean) are representative of two to four mice tested in three independent experiments. (C) Distribution of virus-specific T cells in different organs. Absolute numbers of NP396-specific CD8+ T cells detected with DbNP396 tetramers were calculated by multiplying the fraction of tetramer+ cells among CD8+ T cells by the fraction of CD8+ T cells among live cells, as well as total live spleen cell counts or total pooled (inguinal, mesenteric, axillary, and cervical) lymph node (LN) counts. For an estimate of the total specific CD8+ T cells in blood, the product of the tetramer+ and CD8+ T-cell fractions was multiplied by the white blood cell count per cubic millimeter and a coefficient of 5,850/100 g of body weight. (D) Differential regulation of coreceptor expression. Changes in CD4 and CD8 coreceptor expression on activated T cells 8 days after LCMV is plotted as percent change in the coreceptor geometric mean fluorescence intensity by comparing proliferated (BrdU+) to resting (BrdU) T cells within the same samples.

Dirk Homann, et al. J Virol. 2006 January;80(1):270-280.

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