A low-loss terahertz air-core microstructure fiber is demonstrated for terahertz waveguiding. Substantially low attenuation constant less than 0.01 cm −1 has been achieved and the guiding wavelength is found to be tunable by linear scaling the fiber size. The experimental results well agree with the simulation based on the finite-difference frequency-domain method, which interprets the guiding mechanism as the antiresonant reflecting waveguiding. The simulated modal pattern shows that most terahertz field is concentrated inside the central hollow air core and is guided without outside interference, which has high potential for guiding intense terahertz waves with minimized loss.

We demonstrate a new reflective imaging technique using continuous-wave THz fiber-endoscopy, in which the sample is placed behind the output of a THz subwavelength plastic fiber and the Fabry Perot interference is formed therein. 3D THz reflective images with a reasonable SNR as well as high lateral and subwavelength axial resolutions are acquired by moving the sample along the axial (z) direction and by 2D scanning the output end of the subwavelength plastic fiber without any focusing medium. By analyzing the axial-position dependent THz signals backward collected by the subwavelength plastic fiber, the THz reflection amplitudes and phases on the sample surface can be successfully reconstructed.

By measuring the spectral loss characteristics of subwavelength-diameter terahertz fibers, our study supports the recent theory proposed by M. Sumetsky [Opt. Lett. 31, 870 (2006)] that diameter-variation-induced radiation is a dominant loss mechanism for subwavelength fibers in the low- (<1%) core-fraction-power regime. This physical mechanism limits the lowest guidable frequency in a subwavelength fiber.

The immunomodulatory effect of IL-10 as an immunosuppressive and anti-inflammatory cytokine is well known. Taking advantage of our established mouse model of autoimmune cholangitis using 2-octynoic acid conjugated ovalbumin (2-OA-OVA) induction, we compared liver pathology, immune cell populations and antimitochondrial antibodies between IL-10 knockout and wild type mice immunized with 2-OA-OVA. At 10 weeks post immunization, portal inflammation and fibrosis were more severe in 2-OA-OVA immunized IL-10 knockout mice than in wild type mice. This was accompanied by significant higher levels of collagen I and III expression, T, NK and NKT subsets in liver and IgG anti-mitochondrial autoantibodies (AMA) compared to 2-OA-OVA immunized wild type mice, suggesting that endogenous IL-10 is necessary for the maintenance of immune tolerance in primary biliary cholangitis (PBC). Further, we investigated whether administration of exogenous IL-10 could prevent PBC by administration of IL-10 expressing recombinant adeno-associated virus (AAV-IL-10) either 3 days before or 3 weeks after the establishment of liver pathology. Interestingly, administration of AAV-IL-10 resulted in increased liver inflammation and fibrosis, accompanied by increases in IFN-γ in liver CD4+ T cell, granzyme B, FasL, and CD107a in liver CD8+ T and NKT cells, and granzyme B and FasL in liver NK cells of AAV-IL-10 administered mice compared with control mice. Furthermore, administration of AAV-IL-10 significantly increased levels of proinflammatory cytokines and chemokines (IFN-γ, TNF-α, CXCL9 and CXCL10) and collagen I and III production in naive mice, together with increase in immune cell infiltration and collagen deposition in the liver, suggesting a role of IL-10 in fibrosis. In conclusion, our data demonstrate that endogenous IL-10 is critical in the maintenance of immune tolerance but exogenous administration of IL-10 exacerbates liver inflammation and fibrosis. Furthermore, the distinctive presence of inflammatory immune cell populations and collagen expression in AAV-IL-10 treated naive mice cautions against the clinical use of exogenous IL-10 in patients with autoimmune cholangitis.

No abstract