Radar graphics showing the proportion of subjects and the immunological biomarkers production in infective endocarditis (IE) etiological subgroups.

<p>The subgroups evaluated were: culture-negative IE (CN-IE), non-staphylococcal IE (non-S IE), and staphylococcal IE (S IE). Elevated proportion of high producers of IL-1β, TNF-α and IL-12 was observed only in the S IE subgroup. The prevalence of high producers of IL-10 was lower in the S IE subgroup as compared to the others subgroups.</p

Baseline characteristics of the patients with infective endocarditis.

<p>*Data presented as mean and standard deviation (mean ± SD) or absolute number (percentage) of patients.</p><p>Baseline characteristics of the patients with infective endocarditis.</p

Networks of cytokines associated with Infective endocarditis.

<p>The groups evaluated were: health controls (HC), infections endocarditis (IE) and etiological subgroups: non-staphylococcal IE (non-S IE) and staphylococcal IE (S IE). Biomarkers networks were assembled to assess the association between human cytokines for each clinical group. The biomarkers networks were constructed using circle layouts with each cytokines represented by specific gray-scale globular nodes.</p

Serum concentrations of inflammatory cytokines in the patients with infective endocarditis (IE) stratified according to the microorganisms.

<p>The groups evaluated were: culture-negative IE (CN-IE) (white circle), non-staphylococcal IE (non-S IE) (light gray circle), and staphylococcal IE (S IE) (dark gray circle). Significant differences at p<0.05 are highlighted by letter for difference of a group as compared to non-infective endocarditis indicated by ‘‘b”.</p

Comparison between cytokine levels and major symptoms at diagnosis of infective endocarditis and mortality.

<p>TNF-α, tumor necrosis factor-α.</p><p>*Median (interquartile range), pg/mL.</p><p>Comparison between cytokine levels and major symptoms at diagnosis of infective endocarditis and mortality.</p

Radar graphics showing the proportion of subjects and the immunological biomarkers production in different contexts.

<p>None of the individuals could be identified as high producers of cytokines in the health controls (HC) group. The infective endocarditis (IE) group presented high producers of all cytokines. The non-IE infections group presented high producers of IL-6 and IL-8.</p

Immunological Profile of HTLV-1-Infected Patients Associated with Infectious or Autoimmune Dermatological Disorders

<div><p>In the present study, the frequency, the activation and the cytokine and chemokine profile of HTLV-1 carriers with or without dermatological lesions were thoroughly described and compared. The results indicated that HTLV-1-infected patients with dermatological lesions have distinct frequency and activation status when compared to asymptomatic carriers. Alterations in the CD4⁺HLA-DR⁺, CD8⁺ T cell, macrophage-like and NKT subsets as well as in the serum chemokines CCL5, CXCL8, CXCL9 and CXCL10 were observed in the HTLV-1-infected group with skin lesions. Additionally, HTLV-1 carriers with dermatological skin lesions showed more frequently high proviral load as compared to asymptomatic carriers. The elevated proviral load in HTLV-1 patients with infectious skin lesions correlated significantly with TNF-α/IL-10 ratio, while the same significant correlation was found for the IL-12/IL-10 ratio and the high proviral load in HTLV-1-infected patients with autoimmune skin lesions. All in all, these results suggest a distinct and unique immunological profile in the peripheral blood of HTLV-1-infected patients with skin disorders, and the different nature of skin lesion observed in these patients may be an outcome of a distinct unbalance of the systemic inflammatory response upon HTLV-1 infection.</p></div

Plasmatic levels of chemokines and cytokine ratios among HTLV-1-infected patients with skin lesions.

<p>Serum chemokines and cytokines quantitation were performed by CBA as described in <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002328#s2" target="_blank">materials and methods</a>. The results are expressed as concentration in pg/mL (×10³) ± standard error of (A) CCL2, (B) CCL5, (C) CXCL8, (D) CXCL9, (E) CXCL10 in the serum of HTLV-infected patients and controls with infectious (L^(INF) = dark gray rectangles) and autoimmune (L^(AI) = black-gray rectangles) skin lesions as well as carriers and controls without skin lesions (L⁽⁻⁾ = light gray rectangles). Significant differences at <i>P</i><0.05 are highlighted by letters for difference of a group as compared to control L⁽⁻⁾ indicated by “a”, to control L^(INF) indicated by “b”, to control L^(AI) indicated by “c”, to HTLV-1+ L⁽⁻⁾ indicated by “d” and to HTLV-1+ L^(INF) indicated by “e”. The ratio between cytokines and IL-10 for all groups was calculated for (F) IL-1β, (G) IL-6, (H) IL-12, (I) TNF-α. Significant differences are highlighted by connecting lines.</p

Proviral load of HTLV-1-infected patients without and with infectious or autoimmune skin lesions.

<p>(A) Proviral load was measured by Real Time PCR as described in <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0002328#s2" target="_blank">Materials and Methods</a> and results are expressed in number of HTLV-1 genome copies per 10⁴ peripheral blood mononuclear cells (PBMCs). The frequency of high (black rectangles #6 – 2 without skin lesions and 4 with skin lesions) medium (gray rectangles #11 – 1 without skin lesions and 10 with skin lesions) and low (white rectangles #19 – 6 without skin lesions and 13 with skin lesions) copy number was defined by the global arithmetic mean of all data (B) and individual groups (C).</p

Description of patients included in the cell subset analysis.

#<p>- Age average in years;</p>*<p>M/F – Male/Female ratio.</p