role of th1 and th17 cd4+ t cell subsets in the pathogenesis of ...

experimental autoimmune uveitis (EAU) animal model for autoimmune uveitis in
humans, Th17 cells played a dominant role in the immunization model with the retinal
antigen interphotoreceptor retinoid‐binding protein. However, Th1 cells were able to
induce severe EAE in a transfer model and independently of local IL‐17 (Luger et al.,
2008) showing that the dominant effector T helper cell phenotype in pathological
conditions may be determined by the model. Similarly, the adoptive transfer of either
hen egg lysozyme‐specific Th1 or Th17 cell lineages into hosts expressing hen egg
lysozyme as pseudo autoantigen their eyes induced ocular inflammation but with slight
differences in histological pathology and selective cytokine and chemokine expression,
indicating that Th1 and Th17 might have distinct activities in mediating inflammation
(Cox et al., 2008). More recently, in the experimental model for autoimmune diabetes,
adoptive transfer of Th1 or Th17 cells from BDC2.5 transgenic mice into NOD/SCID
recipient mice induced diabetes with similar rates of onset. Interestingly, a substantial
plasticity of Th17 cell commitment toward a Th1‐like profile was observed in the
NOD/SCID recipients (Bending et al., 2009). In fact, a recent report emphasized the
plasticity of Th17 cells through the use of fluorescent reporter mice for IL‐17F by
showing that Th17 cells convert to a Th1 phenotype when transferred into lymphopenic
hosts but not into normal animals (Nurieva et al., 2009).
In summary, in the past years we have witnessed a real revolution in the understanding
of helper T cell subsets biology and differentiation and their role in pathological
conditions. This subject was found to be more complex than initially thought and too
haste rush was taken in the evaluation of the experimental data, leading to some
confusion in the field.
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1.5 ‐ CHEMOKINES AND CHEMOKINE RECEPTORS
Chemokines and chemokine receptors are important cell migration regulators during an
immune response. Chemokines exert their function via interaction with their cognate
receptors in the target cell, which are G protein‐coupled receptors (GPCRs), thus
activating multiple signaling transduction pathways depending on the cell type.