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We provide evidence that, alongside topologically protected edge states, two-dimensional Chern insulators also support localized bulk states deep in their valence and conduction bands. These states manifest when local potential gradients are applied to the bulk, while all parts of the system remain adiabatically connected to the same phase. In turn, the bulk states produce bulk current transverse to the potential difference. This occurs even when the potential is always below the energy gap, where one expects only edge currents to appear. Bulk currents are topologically protected and behave as edge currents under an external influence, such as temperature or local disorder. Detecting topologically resilient bulk currents offers a direct means to probe the localized bulk states.

Here we provide a general methodology to directly measure the topological currents emerging in the optical lattice implementation of the Haldane model. Alongside the edge currents supported by gapless edge states, transverse currents can emerge in the bulk of the system whenever the local potential is varied in space, even if it does not cause a phase transition. In optical lattice implementations the overall harmonic potential that traps the atoms provides the boundaries of the topological phase that supports the edge currents, as well as providing the potential gradient across the topological phase that gives rise to the bulk current. Both the edge and bulk currents are resilient to several experimental parameters such as trapping potential, temperature, and disorder. We propose to investigate the properties of these currents directly from time-of-flight images with both short-time and long-time expansions.

Aim: This study aims to demonstrate that HLA-DR15 blockade inhibits auto reactivity to the immunodominant T-cell epitope, alpha3135-145 and attenuates disease in experimental autoimmune anti-glomerular basement membrane (GBM) disease. Background(s): Anti-GBM disease is an autoimmune disease that manifests as rapidly progressive glomerulonephritis. It has a strong HLA association with the DR15 allele (odds ratio: 8.5) and the immunodominant, DR15-restricted T-cell epitope has been defined. A DR15-specific inhibitor, PV-267, has potential as a targeted therapy, as current treatments are nonspecific and have detrimental side effects. Method(s): HLA-DR15 transgenic mice were used to examine the potential of PV-267 in attenuating DR15-mediated autoreactivity and disease. Autoreactivity to alpha3135-145 was determined by immunizing mice with alpha3135-145, then measuring recall responses ex vivo 10 days later by 3[H]-T proliferation and IFN-gamma and IL-17 ELISPOTs. Experimental autoimmune anti-GBM disease was induced by immunizing mice (backcrossed onto an FcgammaRIIb-/- background) with three weekly injections of alpha3135-145; functional and histological endpoints, as well as immune cell infiltration, were determined at 6weeks. Result(s): Compared with mice that received vehicle control, DR15 transgenic mice that received PV-267 daily (30mg/kg) from day 1 had reduced alpha3135-145-specific proliferation (SI: 9.5 +/- 0.9 vs 2.2 +/- 0.5, P<0.001) as well as reduced numbers of IFN-gamma and IL-17 spots. In experimental anti-GBM disease, DR15 transgenic mice that received PV-267 (30mg/kg) on alternate days from day 1 had fewer infiltrating glomerular Tcells (cells/glomerular cross section: 0.90+/- 0.12 vs 0.36+/- 0.03, P<0.01), reduced 24-hour albuminuria (mug: 1064+/- 313 vs 42+/- 29, P<0.01), and reduced glomerular segmental necrosis and crescent formation. Conclusion(s): HLA-DR15 inhibition effectively attenuates experimental autoimmune anti-GBM disease and highlights t