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Picard C, Casanova JL » «
Secretion of IL-17 by T cell blasts from controls (black circles) and patients (red circles), as measured by ELISA.
Patients with STAT-3 deficiency had the most severe IL-17 phenotype of all the patients tested, with a profound impairment of IL-17 production by T cells ex vivo and T cell blasts in vitro.
S3 shows the secretion of IL-22 by T cell blasts from controls and patients in the various culture conditions, as measured by ELISA.
These data indicate that STAT-3 is required for the maintenance and expansion of IL-17–secreting human T cell blasts and for the secretion of IL-22 by human T cell blasts, at least in these experimental conditions.
In patients, most of the IL-17 producing T-cells were confined to the CCR6+ T-cell subset (80 ± 13%).
Patients with and without active disease were analysed for CD80 expression on IL-17 producing T-cells.
Percentages of IL-17 expressing T-cells were significantly increased in patients with active disease as compared to healthy controls (1.46 ± 0.58% versus 0.93 ± 0.30%, P = 0.007).
The percentage of IL-17 producing T-cells was analysed in the peripheral blood of 30 SLE patients and 16 healthy controls.
Although Th17 and Treg differentiation are controlled by reciprocal molecular pathways, naïve T cells activated with TGF-β and IL-6 can differentiate into Th17 cells in the presence of nTreg , , .
CD28 co-stimulation inhibits in vitro generation of IL-17 producing CD4+ T cells.
As shown in the percentage of CD4+ T cells producing IL-17 was significatively augmented with high doses of immobilized anti-CD3 mAb.
In agreement with these observations, we found that the enhancement in IFN-γ and IL-2-secreting CD4+ T cells was inversely correlated with the frequency of IL-17-producing cells.
The finding that vitamin A deficiency promotes increased development of Il10-expressing T cells in vivo supports the role of at-RA in suppressing development of IL-10–competent T cells, particularly the Foxp3− IL-10–competent Tr1-type subset.
Il10-competent CD4 T cells stimulated ex vivo produced a substantial amount of IL-10 protein (1.7 ± 0.1 ng/ml) ().
Importantly, we saw very little expression of IL-17 by CD4 T cells activated with CpG-BMDC in the presence of TGF-β, even when blocking antibodies against IFN-γ and IL-4 were included ().
Concerning T cells that coexpress Foxp3 and Il10, although rapid induction of this phenotype was observed in a minor fraction of naive CD4 T cells activated with TGF-β and IL-6 under conditions of limited at-RA in vitro, we have previously shown that Foxp3+IL-10+ T reg cells arise in the periphery from Foxp3+IL-10− precursors, especially in intestinal tissues ().
The mice that received the T cells differentiated with IL-12 or IL-1β + IL-23 developed severe EAE ().
Because IFN-γ–deficient mice develop EAE and develop encephalitogenic Th17 and not Th1 cells, we examined whether the CNS-infiltrating T cells coexpressed IL-17 and T-bet.
As seen in , many combinations of these cytokines generated T cells capable of producing IL-17.
Encephalitogenic T cells differentiated in vitro with IL-12 or IL-1β + IL-23 expressed high levels of T-bet, whereas addition of TGF-β consistently reduced T-bet expression and encephalitogenic capacity.
Moreover, the frequency of IL-17-producing T cells is increased in the peripheral blood of patients with SLE [, , ].
In these mice as in the MRL/lpr, IL-17-producing T cells are detected in kidneys affected by nephritis.
The immune environment in patients with SLE is ideally suited for the generation of IL-17-producing T cells.
Support for their pathogenic role derives from the fact that IL-17-producing T cells have been observed in kidneys of patients with lupus nephritis [, ], among infiltrates rich in DN T cells [].
These data show for the first time that the formation of IL-17A and RORγt-expressing TCRγδ+ T cells is IL-23 dependent in vivo.
Therefore, studies on early RA patient materials including synovial tissue infiltrates are needed to evaluate the presence of IL-17-producing TCRγδ T cells.
Here, we found a relatively high percentage of IL-17-producing TCRγδ+ T cells in the spleen and inflamed joints of arthritic wild type mice.
These data show that IL-23 is critical for full-blown expression of a non-autoimmune destructive arthritis and regulates the proportion of IL-17A and IFN-γ-positive CD4+ T cells at the site of inflammation.
Successful allergen-specific immunotherapy (SIT) is associated with reduced Th2 cytokine production and the induction of IL-10-producing regulatory T cells.
This was associated with decreased IL-4 and IL-5 levels, and increased IL-10 levels in BAL fluids as well as increased amounts of IL-10-producing CD25+ regulatory T cells.
Furthermore, CD4 CD25 double-positive spleen T cells were checked for intracellular IL-10 production by flow cytometry.
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