Sunda-Banda arc transition: incipient continent-island arc collision (Northwest Australia)

The eastern Sunda arc represents one of the few regions globally where the early stages of continent-arc collision can be studied. We studied along the western limit of the collision zone at the Sunda-Banda arc transition, where the Australian margin collides with the Banda island arc, causing widespread back arc thrusting. We present integrated results of a refraction/wide-angle reflection tomography, gravity modeling, and multichannel reflection seismic imaging using data acquired in 2006 southeast of Sumba Island. The composite structural model reveals the previously unresolved deep geometry of the collision zone. Changes in crustal structure encompass the 10 - 12 km thick Australian basement in the south and the 22 - 24 kmthick Sumba ridge in the north, where backthrusting of the 130 km wide accretionary prism is documented. The structural diversity along this transect could be characteristic of young collisional systems at the transition from oceanic subduction to continent-arc collision. Citation: Shulgin, A., H. Kopp, C. Mueller, E. Lueschen, L. Planert, M. Engels, E. R. Flueh, A. Krabbenhoeft, and Y. Djajadihardja (2009), Sunda-Banda arc transition: Incipient continent-island arc collision (northwest Australia), Geophys. Res. Lett., 36, L10304, doi: 10.1029/2009GL037533

Cross-Priming of Naive Cd8 T Cells against Melanoma Antigens Using Dendritic Cells Loaded with Killed Allogeneic Melanoma Cells

The goal of tumor immunotherapy is to elicit immune responses against autologous tumors. It would be highly desirable that such responses include multiple T cell clones against multiple tumor antigens. This could be obtained using the antigen presenting capacity of dendritic cells (DCs) and cross-priming. That is, one could load the DC with tumor lines of any human histocompatibility leukocyte antigen (HLA) type to elicit T cell responses against the autologous tumor. In this study, we show that human DCs derived from monocytes and loaded with killed melanoma cells prime naive CD45RA+CD27+CD8+ T cells against the four shared melanoma antigens: MAGE-3, gp100, tyrosinase, and MART-1. HLA-A201+ naive T cells primed by DCs loaded with HLA-A201− melanoma cells are able to kill several HLA-A201+ melanoma targets. Cytotoxic T lymphocyte priming towards melanoma antigens is also obtained with cells from metastatic melanoma patients. This demonstration of cross-priming against shared tumor antigens builds the basis for using allogeneic tumor cell lines to deliver tumor antigens to DCs for vaccination protocols