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1.
Figure 2

Figure 2. From: Reciprocal function of G?i2 and G?i3 in graft-versus-host disease.

Histological examination of diseased liver and colons. (A) Shown are representative H & E-stained sections of the liver from mice reconstituted with WT T cells (i and ii) for 35 days, Gαi2−/− T cells (iii and iv) for 35 days or Gαi3−/− T cells (v, vi, and vii) for 21 days described in Fig. 1. Arrows indicate bile duct damage. The panels ii, iv, and vi (200X) and vii (600X) are the enlargement of i, iii, or v (100X), respectively. (B) Representative H&E-staining of colonic mucosa of the mice described in (A). Arrows indicate crypt abscesses and apoptosis in Gαi3−/− T cell-infused mice or apoptosis in mice adoptively transferred with WT T cells. The magnifications are 200X for the top three sections and 600X for the enlarged section of the colon from Gαi3−/− T cell-infused mice in the lower panel.

Yong Zhu Jin, et al. Eur J Immunol. ;38(7):1988-1998.
2.
Figure 7

Figure 7. From: Reciprocal function of G?i2 and G?i3 in graft-versus-host disease.

Chemotactic responses of activated T cells in the presence vs. absence of Gαi2 or Gαi3. T cells isolated from the indicated mice were either stimulated for 6 days with irradiated splenocytes isolated from SCID BALB/c mice (A and B) or stimulated with ConA for 4 days (C). Chemotaxis of the resultant cells was assayed as in Fig. 6A. Data are presented as mean chemotactic indexes ± SD of cell migration toward CXCL10 (A), CXCL11 (B), and CCL5 (C) relative to control medium. Cumulative data from at least six (A) or three (B and C) experiments with each in triplicate are shown. Statistic significance (*p<0.05 or **p<0.01) in the presence vs. absence of a specific Gαi protein.

Yong Zhu Jin, et al. Eur J Immunol. ;38(7):1988-1998.
3.
Figure 1

Figure 1. From: Reciprocal function of G?i2 and G?i3 in graft-versus-host disease.

Reciprocal effects of Gαi2 and Gαi3 on GVHD development. SCID BALB/c mice were each administrated intraperitoneally with 107 T cells isolated from WT, Gαi2−/−, and Gαi3−/− mice on 129Sv/C57BL/6 background. Animals were monitored for weight (A) and survival (B) weekly. Note: significant acceleration of GVHD-associated morbidity in recipient of Gαi3−/− T cells (**p<0.01) and reduction of the disease in recipient of Gαi2−/− T cells (*p<0.05) as compared to mice receiving WT T cells. Results are from three (Gαi3−/− T cells) or four (Gαi2−/− T cells) independent experiments with 7∼12 mice per group in each experiment. The total number of mice was 31, 28 and 30 receiving WT, Gαi2−/− and Gαi3−/− T cells, respectively. Mean ± SD of weight changes relative to day 0 is shown in (A) (*p<0.05).

Yong Zhu Jin, et al. Eur J Immunol. ;38(7):1988-1998.
4.
Figure 4

Figure 4. From: Reciprocal function of G?i2 and G?i3 in graft-versus-host disease.

Differential proliferation of donor T cells in the presence or absence of a Gαi protein. Mice reconstituted with CFSE-labeled T cells prepared from indicated mice as described in Fig. 3 were sacrificed at days 10 (A) or 25 (B). CFSE fluorescence intensity was analyzed by flow cytometry on gated CD3+ T cells in different tissues. The numbers within each histogram indicate percentages of CFSE-bright and CFSE-dim cell populations, respectively. One representative result of nine mice with similar results is shown for each tissue. SPL, spleen; PLN, peripheral lymph nodes; MLN, mesenteric lymph nodes; LNG, lung; LIV, liver; INS, intestine; and COL, colon.

Yong Zhu Jin, et al. Eur J Immunol. ;38(7):1988-1998.
5.
Figure 6

Figure 6. From: Reciprocal function of G?i2 and G?i3 in graft-versus-host disease.

Chemotactic responses of non-stimulated T cells in the presence or absence of a Gαi protein. (A) T cells freshly isolated from WT, Gαi2−/− and Gαi3−/− mice were added to the upper chamber and S1P at the indicated concentrations was added to the lower chamber. After 4-h incubation, the migrated cells in the lower chamber were counted and expressed as mean chemotactic indexes ± SD of cell migration toward S1P relative to control medium as defined in the Materials and methods. (B and C) T cells isolated from indicated mice, along with 500 nM S1P, were added to the upper chamber and varying concentrations of CXCL12 (B) and CCL21 (C) were added to the lower chamber. Migration was assayed as in (A) and data are presented as mean chemotactic indexes ± SD of cell migration toward CXCL12 or CCL21 relative to control medium. Cumulative data from at least six (A) or three (B and C) experiments with each in triplicate are shown. Statistic significance (*p<0.05 or **p<0.01) in the presence vs. absence of a specific Gαi protein.

Yong Zhu Jin, et al. Eur J Immunol. ;38(7):1988-1998.
6.
Figure 3

Figure 3. From: Reciprocal function of G?i2 and G?i3 in graft-versus-host disease.

Effects of Gαi2 and Gαi3 on donor T cell tissue distribution at indicated times after adoptive transfer. T cells isolated from WT, Gαi2−/− or Gαi3−/− mice were labeled with CFSE and injected into SCID BALB/c mice at a dose of 107 T cells/mouse. The total numbers of donor T cells in different tissues were obtained on the basis of percentages of CD3+ cells at days 1 (top), 10 (middle), 25 (low), and 35 (inset in the lower panel). Donor T cells in the cavity lavage were also shown after 6 and 12 h injection (top right panel). BLD, blood; SPL, spleen; PLN, peripheral lymph nodes; MLN, mesenteric lymph nodes; LNG, lung; LIV, liver; INS, intestine; and COL, colon. Results are the mean ± SD of three independent experiments each with three mice per time point (n=9 at each time point). *p<0.05 or **p<0.01 as analyzed by a Wilcoxon signed rank test.

Yong Zhu Jin, et al. Eur J Immunol. ;38(7):1988-1998.
7.
Figure 5

Figure 5. From: Reciprocal function of G?i2 and G?i3 in graft-versus-host disease.

Enhanced trafficking of Gαi3-deficient T effectors to inflammatory sites in early GVHD hosts. Gαi2- or Gαi3-KO T cells and WT T cells activated by MHC-mismatched hosts were isolated, stained with a fluorescent dye TRITC or CFSE, respectively, mixed at a 1:1 ratio, and injected into SCID mice that had been primed by WT T cells for three weeks as detailed in the Materials and methods. Distribution of Gαi2- or Gαi3-KO T cells relative to WT T cells in different tissues was analyzed at 1 or 18 h after T cell transfer. Homing efficiency in the presence or absence of a specific Gαi protein is expressed as homing indices where homing index for WT T cells is normalized to 1 (dash line). Data shown are the means ± SD for seven mice at each time point in two separate experiments. BM, bone marrow; PLN, peripheral lymph nodes; MLN, mesenteric lymph nodes; *p<0.05, **p<0.01 compared to WT control T cells.

Yong Zhu Jin, et al. Eur J Immunol. ;38(7):1988-1998.

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