T_H17 cell antigens isolated from immunogenic fractions of soluble portion of RM200, predicted function, and primers used for expression in <i>E. coli.</i>

<p>T_H17 cell antigens isolated from immunogenic fractions of soluble portion of RM200, predicted function, and primers used for expression in <i>E. coli.</i></p

Immunization with individual proteins confers protection against nasopharyngeal carriage.

<p>Mice were intranasally immunized twice with 1 µg of cholera toxin alone (CT) or CT combined with the proteins as indicated. Four weeks after the second immunization, mice were intranasally challenged with strain 0603; density of colonization was determined one week later. Bars indicate median values and nasal colonization density was compared by the Mann-Whitney <i>U</i> test.</p

Size separation of fractions and stimulation of splenocytes.

<p>A. SDS-PAGE of fractions was performed and gel was silver-stained; shown here are the electrophoretic patterns of three fractions eluted into the same chamber during different transverse elutions. B. Results from stimulation of splenocytes from WCC immunized mice (n = 6) with equal concentrations of each fraction. Supernatants were collected after 3 days of incubation and IL-17A concentration in the supernatant was measured by ELISA. IL-17A values are shown here, normalized to the DMEM-stimulated response of each animal. Bars represent medians with interquartile range. WCC: chloroform-inactivated pneumococcal whole cell antigen, 10 µg protein/ml; WCCsup: soluble fraction of WCC, 7 µg protein/ml.</p

Stimulation of splenocytes from immune mice with purified recombinant proteins.

<p>Mice (n = 7–10) were intranasally immunized with WCC and cholera toxin as described. Splenocytes from immunized mice were stimulated with 10 μg/ml of the indicated recombinant protein for 3 days, after which supernatants were harvested and assayed for IL-17A concentration. Values are normalized to the DMEM stimulated response for each animal. Bars represent medians with interquartile ranges.</p

Immunological mechanisms of control of pneumococcal carriage.

<p>The serotype-dependent and -independent immunological mechanisms that control pneumococcal carriage are depicted. Memory B cells and plasma cells specific to capsule and proteins produce IgG. This can lead to antibody-mediated pneumococcal agglutination and antibody-mediated phagocytosis by neutrophils, monocytes, and macrophages. Moreover, IL-17A produced by memory CD4⁺ T cells might lead to recruitment and activation of neutrophils and monocytes/macrophages, thus increasing phagocytosis. CCL2, C-C motif chemokine ligand 2; CD4⁺, cluster of differentiation 4; IgG, immunoglobulin G; IL-17A, interleukin 17-A.</p

Box-Whisker Plot of Anti-Type-14 Polysaccharide Antibodies in Israeli Toddlers, by 6-Mo Age Groups

<p>Central boxes indicate median and 25th and 75th percentiles; whiskers indicate upper and lower adjacent values.</p

Age-Specific Incidence of Invasive Pneumococcal Disease in the United States by Serogroup, Based on Data from Active Bacterial Core Surveillance

<p>Serogroups 4 and 23 are shown only up to 48 mo, after which incidence is less than 1/100,000 person-years. All serogroups besides those in the heptavalent vaccine are shown combined as non-vaccine serogroups (NVG).</p

Age-Specific Incidence of Invasive Pneumococcal Disease in the United States by Disease Type, Based on Data from Active Bacterial Core Surveillance

<p>Meningitis incidence is plotted only up to 30 mo, after which it remains at or below 1/100,000 person-years. “Pneumonia” indicates bacteremic pneumonia, while “bacteremia” indicates nonfocal bacteremia. “Total” includes other invasive diagnoses.</p

Age-Specific Incidence of Invasive Pneumococcal Disease Caused by Serogroups 6 and 14 in Finland, Based on Active Laboratory-Based Surveillance

<p>Age-Specific Incidence of Invasive Pneumococcal Disease Caused by Serogroups 6 and 14 in Finland, Based on Active Laboratory-Based Surveillance</p

Cytokine expression by Foxp3+ Treg in adenoidal cells.

<p>Percentage of Foxp3+ Treg in adenoidal MNC after stimulation with WCA compared with unstimulated medium control (A). Intracellular cytokine staining shows IL-10 (B) and IL-17 (C) production by Foxp3+ Treg and Foxp3− CD4+ T cells after WCA stimulation compared with unstimulated control. Only CD4+ T cell gate is shown in B and C. Result of one representative experiment of four replicates is shown.</p