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Many studies reported the production of IL-17 by Treg cells, associated with a decrease in Foxp3 and a concomitant increase in Ror γt (or Rorc in human) expressions [ 38– 40], thus demonstrating a switch toward Th17 cell subset ex vivo and in vivo.
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This lends support to Pollyanna hypothesis [3] that there should be a positive bias in human expression.
If regulators of HML-2 transcription were differentially expressed in humans expression levels of those regulators could indirectly result in differential HML-2 expression levels.
MalarImDB allows comparisons between expression levels in humans, expression levels in murine models, and functional data from experimental treatments in mice.
IL-17 expression may be completely extinguished such that Th-17 cells develop a Th-1 phenotype, though in humans, expression of the Th-17 marker CD161 is maintained on these "converted" cells [40].
Similar to ADAMTS16 in humans, expression of Adamts16 was prominent in the kidney.
In humans, expression of hemopexin has been previously reported in neuroretina and glial cell (15, 16).
In humans, expression of THRSP in adipose tissue is depressed by transition from a lipogenic fed state to a lipolytic state induced by a 48 hr fast [ 115].
In humans, expression of KCNH2-1a, a gene coding for a hERG channel subunit present in cardiac tissues, has been reported also in the hippocampus and cerebral cortex.
Why are CIDE knockout mice protected from obesity and insulin resistance whereas in humans, expression levels inversely correlate with insulin sensitivity?
In humans, expression of an asporin variant with a high TGF-beta inhibitory effect is significantly correlated with an increased incidence of OA [ 19].
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