Figure 6
Figure 6. In vivo blockade of α4β7-integrin dampens pDC recruitment and reduces immune activation in the colorectum of SIV-infected RMs after intrarectal infection. (A) Frequency of pDCs in colorectum of the untreated control group and anti–α4β7-integrin antibody-treated group. Asterisk (*) indicates significant difference between groups at week 2 PI (P = .02). Frequency of Ki-67+ CD8 T cells (B) and Ki-67+ CD4 T cells (C) in the colorectum post-SIV infection. Charts show the geomean and individual data from the treated and untreated groups. An average of 3 preinfection time points was used for week 0. The increase in Ki-67+ CD8 or CD4 T cells was calculated by subtracting the proportion of these cells at week 0 from the proportion of Ki-67+ CD8 or CD4 T cells at a specific postinfection time point. P values (0.03 or 0.049) indicate significant difference between groups at week 3 PI for CD8 T cells or at week 2 PI for CD4 T cells. (D) Association between pDC frequency in the colorectum and the increase in Ki-67+ CD8 or CD4 T-cell levels in the colorectum at week 2 or week 3 postinfection. Data are obtained from treated and untreated groups. Nonparametric correlation was analyzed using the Spearman 2-tailed test. (E) Relative fold increase of MX1 or OAS2 mRNA levels in the colorectum of untreated and treated RMs at week 3 PI. Relative fold increase gene expression is calculated using week 3 PI levels over preinfection levels. (F) Association between pDC frequency in the colorectum at week 3 PI and MX1 or OAS2 fold-increase gene expression levels in the colorectum at week 3 PI. Data are obtained from treated and untreated groups. Nonparametric correlation was analyzed using the Spearman 2-tailed test.

In vivo blockade of α4β7-integrin dampens pDC recruitment and reduces immune activation in the colorectum of SIV-infected RMs after intrarectal infection. (A) Frequency of pDCs in colorectum of the untreated control group and anti–α4β7-integrin antibody-treated group. Asterisk (*) indicates significant difference between groups at week 2 PI (P = .02). Frequency of Ki-67+ CD8 T cells (B) and Ki-67+ CD4 T cells (C) in the colorectum post-SIV infection. Charts show the geomean and individual data from the treated and untreated groups. An average of 3 preinfection time points was used for week 0. The increase in Ki-67+ CD8 or CD4 T cells was calculated by subtracting the proportion of these cells at week 0 from the proportion of Ki-67+ CD8 or CD4 T cells at a specific postinfection time point. P values (0.03 or 0.049) indicate significant difference between groups at week 3 PI for CD8 T cells or at week 2 PI for CD4 T cells. (D) Association between pDC frequency in the colorectum and the increase in Ki-67+ CD8 or CD4 T-cell levels in the colorectum at week 2 or week 3 postinfection. Data are obtained from treated and untreated groups. Nonparametric correlation was analyzed using the Spearman 2-tailed test. (E) Relative fold increase of MX1 or OAS2 mRNA levels in the colorectum of untreated and treated RMs at week 3 PI. Relative fold increase gene expression is calculated using week 3 PI levels over preinfection levels. (F) Association between pDC frequency in the colorectum at week 3 PI and MX1 or OAS2 fold-increase gene expression levels in the colorectum at week 3 PI. Data are obtained from treated and untreated groups. Nonparametric correlation was analyzed using the Spearman 2-tailed test.

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