Abstract
The article by Faal et al. [1] describes differences in the level of FOXP3 mRNA expression in the conjunctiva of patients with Chlamydia trachomatis infection. The authors suggest that their results may indicate a role for regulatory T cells in the resolution of conjunctival immune response, since FOXP3 mRNA remained elevated even if clinical disease signs were present in the absence of infection. But suggestions about the function of regulatory T cells in diseases based only on the quantification of FOXP3 mRNA should be considered with great caution. According to the current state-of-the-art it is well established that FOXP3 does not specify human regulatory T cells since it is expressed at the mRNA and the protein levels to different extents protein at [2–5]. Thus, without quantification of FOXP3 the single cell level in conjunction with reliable markers of human regulatory T cells, e.g., the recently identified lack of CD127 expression on regulatory T cells [6,7], the potential contribution or association of regulatory T cells with a disease cannot be assessed.
Highlights
The core of this study’s results lies in the observation that the 2001–2002 influenza epidemic immediately following 9/11 was late in the season and peaked in March, whereas the eight surrounding epidemics peaked between the end of December and the end of February
Given the complexities of influenza virus subtype cycling and antigenic drift [5,6], it is essential to consider longerterm disease data spanning much more than nine years to interpret the “lateness” of the 2001–2002 epidemic
During the earlier part of the last century when air traffic was minimal, influenza epidemics rapidly circulated around the world
Summary
In addition to comparing the timing of influenza epidemics across different seasons, Brownstein et al analyzed the rate of disease spread among US administrative regions for their nine seasons of interest (1996–2005). We reported the first empirical and quantitative evidence for the effect of airline travel on the rate of epidemic influenza spread.
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