Clinical characteristics of patients with recurrent invasive pneumococcal disease.

<p>P, patient identification; PCV-7, 7-valent polysaccharide-protein conjugate vaccine; PCV 13, 13-valent polysaccharide-protein conjugate vaccine; PPV-23, 23-valent pneumococcal polysaccharide vaccine.</p><p>Clinical characteristics of patients with recurrent invasive pneumococcal disease.</p

Microbiological characteristics of patients with recurrent invasive pneumococcal disease.

<p>P, patient identification; ST, sequence type by Multi-locus sequence typing; MDR, Multi-drug resistant strain; PCV-7, 7-valent polysaccharide-protein conjugate vaccine; PCV 13, 13-valent polysaccharide-protein conjugate vaccine; PPV-23, 23-valent pneumococcal polysaccharide vaccine; CSF, cerebrospinal fluid; NA, Not available; MIC, minimal inhibitory concentration; Pen, penicillin; Ery, erythromycin; Cm, chloramphenicol; Tet, tetracycline; Ctx, Cefotaxime; Bold text, resistant strain according to MICs for <i>Streptococcus pneumonia</i>. EUCAST Clinical Meningeal Breakpoints.</p><p>^aNA, ST were not available in episodes identified only by PCR.</p><p>Microbiological characteristics of patients with recurrent invasive pneumococcal disease.</p

HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4-6

ICAM-3, total LFA-1, the activated form of LFA-1 and CD4. Staining of the cell surface molecules was performed using monoclonal antibodies RM3A5, 140.11, R7.1, mAb24 and Leu3a respectively. The expression of HIV Env was evaluated in MOLT cells using pooled serums from HIV infected individuals. Figure shows the expression of each individual antigen (empty peaks) with the negative control of staining (solid peaks). Histograms show a single representative experiment.<p><b>Copyright information:</b></p><p>Taken from "HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4"</p><p>http://www.retrovirology.com/content/5/1/32</p><p>Retrovirology 2008;5():32-32.</p><p>Published online 31 Mar 2008</p><p>PMCID:PMC2359761.</p><p></p

HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4-0

ICAM-3, total LFA-1, the activated form of LFA-1 and CD4. Staining of the cell surface molecules was performed using monoclonal antibodies RM3A5, 140.11, R7.1, mAb24 and Leu3a respectively. The expression of HIV Env was evaluated in MOLT cells using pooled serums from HIV infected individuals. Figure shows the expression of each individual antigen (empty peaks) with the negative control of staining (solid peaks). Histograms show a single representative experiment.<p><b>Copyright information:</b></p><p>Taken from "HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4"</p><p>http://www.retrovirology.com/content/5/1/32</p><p>Retrovirology 2008;5():32-32.</p><p>Published online 31 Mar 2008</p><p>PMCID:PMC2359761.</p><p></p

HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4-1

Ls appear as an unstained population with high forward scatter values (in orange); while CD4 T cells were identified by fluorescent staining and low forward scatter values (in purple). Events displaying bright fluorescence and forward scatter values consistent with MOLT cells were defined as cellular conjugates (in red, gate MOLT-CD4 in the figure). The percentage of CD4 T cells forming conjugates in the absence or the presence of Leu3a, or under continuous shacking condition is shown in each plot. Panel B shows the quantification of cellular conjugates in the presence of the following inhibitors: mAbs against the adhesion molecules ICAM-1 (RM3A5), ICAM-3 (140.11) and LFA-1 (R7.1), coreceptor antagonists AMD3100 and TAK779 (all at 10 μg/ml), gp41 inhibitor C34 (1 μg/ml) or Leu3a (5 μg/ml). Data are Mean ± SD of 3 independent experiments including cells from 3 different donors. Asterisks indicate a significant inhibition in the formation of conjugates in the presence of Leu3a and under shaking conditions.<p><b>Copyright information:</b></p><p>Taken from "HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4"</p><p>http://www.retrovirology.com/content/5/1/32</p><p>Retrovirology 2008;5():32-32.</p><p>Published online 31 Mar 2008</p><p>PMCID:PMC2359761.</p><p></p

HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4-4

Fied primary CD4 T cells. After 2 h of coculture, cells were stained with anti-CD45RO and anti-HIV p24 antibodies. Analysis of HIV transfer in the absence (left graph) or presence (right graph) of the RM3A5 blocking mAb against ICAM-1 was performed after gating separately CD45RO and CD45RA CD4 T cells. Panel B shows the expression of HIV Env (right) and ICAM-1 (left) in 293T transfected cells (empty peaks), solid peaks correspond to negative controls of staining. Panel C shows HIV transfer from 293T cells transfected with an Env defective and an NL4-3 Env plasmids, to CD45RO- (RO-) and CD45RO+ (RO+) target cells in the absence (light bars) or presence (grey bars) of ICAM-1 expression. HIV transmission was again measured in the absence (left graph) or the presence (right graph) of the blocking RM3A5 antibody against ICAM-1. Values are Mean ± SD of 3 experiments performed with CD4 T cells from 3 different donors. Asterisks denote significant differences in HIV transmission to the CD45RA CD4 T subset compared to CD45RO cells (Panel A and C). Significant differences intrasubsets induced by ICAM-1 expression are also indicated by asterisks in panel C, while ns denotes no statistical significance.<p><b>Copyright information:</b></p><p>Taken from "HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4"</p><p>http://www.retrovirology.com/content/5/1/32</p><p>Retrovirology 2008;5():32-32.</p><p>Published online 31 Mar 2008</p><p>PMCID:PMC2359761.</p><p></p

HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4-3

Ted in each histogram. Control histogram corresponds to background of staining. Panel B shows HIV transfer from 293T cells, transfected to produce HIV particles, to target CD4 T cells in the absence (light bars) or presence (grey bars) of NL4-3 Env expression. The effect on the addition of blocking antibodies against CD4 (Leu3a) and the gp41 inhibitory peptide C34 was also tested. Data (Mean ± SD) were obtained using cells from 3 different donors. Asterisk indicates a significant inhibition in HIV transmission in the presence of Leu3a within NL4-3 Env transfected 293T cells.<p><b>Copyright information:</b></p><p>Taken from "HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4"</p><p>http://www.retrovirology.com/content/5/1/32</p><p>Retrovirology 2008;5():32-32.</p><p>Published online 31 Mar 2008</p><p>PMCID:PMC2359761.</p><p></p

HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4-5

Ure. Cells were gated as CD3+/CD8-/CD4+ PBMCs (non-productively infected cells, upper histograms) or CD3+/CD8-/CD4- PBMCs (productively infected cells, lower histograms). Histograms show a representative experiment displaying the expression of each individual antigen (solid peaks) with the negative control of staining (empty peaks). In panel B, purified productively HIV infected CD3+/CD8-/CD4- PBMCs were cocultured with CMFDA-labeled primary unstimulated CD4 T cells. After 24 hours of coculture cells were stained with anti-CD45RO and anti-HIV CA p24 antibodies. HIV transmission was measured in both memory CD45RO+ (RO+ solid bars) and naive (RO-, empty bars) subsets in the presence of Leu3a, C34 and a panel of blocking agents against adhesion molecules used at the same concentrations as in Figure 3 (whole IgGs against ICAM-1, LFA-1 and ICAM-3, soluble ICAM-1 or Fab fragments of the anti-ICAM-3 mAb 140.11). Values are Mean ± SD of data corresponding to up to 6 different donors. Asterisks indicate significant differences (p < 0.05) from control or between divalent and monomeric blocking agents.<p><b>Copyright information:</b></p><p>Taken from "HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4"</p><p>http://www.retrovirology.com/content/5/1/32</p><p>Retrovirology 2008;5():32-32.</p><p>Published online 31 Mar 2008</p><p>PMCID:PMC2359761.</p><p></p

HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4-2

Ry CD4 T cells with uninfected MOLT (white bars), MOLT NL4-3 (grey bars) or MOLT BaL cells (dark bars). Concentrations were 10 μg/mL for all mAbs against cell surface molecules, except for Leu3a (5 μg/mL) and C34 (1 μg/mL). Data are Mean ± SD of 3 independent experiments employing cells of 3 different donors. Asterisks indicate a significant inhibition in HIV transmission in the presence of Leu3a.<p><b>Copyright information:</b></p><p>Taken from "HIV transfer between CD4 T cells does not require LFA-1 binding to ICAM-1 and is governed by the interaction of HIV envelope glycoprotein with CD4"</p><p>http://www.retrovirology.com/content/5/1/32</p><p>Retrovirology 2008;5():32-32.</p><p>Published online 31 Mar 2008</p><p>PMCID:PMC2359761.</p><p></p

Oxidative burst capacity of neutrophils.

<p>Panel A and B show the burst rate (B-R) in patients treated with triple therapy and IFN-free regimen, respectively. Panel C and D show the enzymatic activity per cell (median fluorescence intensity, B-MFI) in patients treated with triple therapy and IFN-free regimen, respectively. Data are analyzed at baseline (before starting antiviral therapy), and at week 4 and 8 of therapy. * These comparisons were performed by Friedman tests.</p