Facing the threat of influenza pandemic - roles of and implications to general practitioners

The 2009 pandemic of H1N1 influenza, compounded with seasonal influenza, posed a global challenge. Despite the announcement of post-pandemic period on 10 August 2010 by theWHO, H1N1 (2009) virus would continue to circulate as a seasonal virus for some years and national health authorities should remain vigilant due to unpredictable behaviour of the virus. Majority of the world population is living in countries with inadequate resources to purchase vaccines and stockpile antiviral drugs. Basic hygienic measures such as wearing face masks and the hygienic practice of hand washing could reduce the spread of the respiratory viruses. However, the imminent issue is translating these measures into day-to-day practice. The experience from Severe Acute Respiratory Syndrome (SARS) in Hong Kong has shown that general practitioners (GPs) were willing to discharge their duties despite risks of getting infected themselves. SARS event has highlighted the inadequate interface between primary and secondary care and valuable health care resources were thus inappropriately matched to community needs

Apoptotic cell-based therapies against transplant rejection: role of recipient’s dendritic cells

One of the ultimate goals in transplantation is to develop novel therapeutic methods for induction of donor-specific tolerance to reduce the side effects caused by the generalized immunosuppression associated to the currently used pharmacologic regimens. Interaction or phagocytosis of cells in early apoptosis exerts potent anti-inflammatory and immunosuppressive effects on antigen (Ag)-presenting cells (APC) like dendritic cells (DC) and macrophages. This observation led to the idea that apoptotic cell-based therapies could be employed to deliver donor-Ag in combination with regulatory signals to recipient’s APC as therapeutic approach to restrain the anti-donor response. This review describes the multiple mechanisms by which apoptotic cells down-modulate the immuno-stimulatory and pro-inflammatory functions of DC and macrophages, and the role of the interaction between apoptotic cells and APC in self-tolerance and in apoptotic cell-based therapies to prevent/treat allograft rejection and graft-versus-host disease in murine experimental systems and in humans. It also explores the role that in vivo-generated apoptotic cells could have in the beneficial effects of extracorporeal photopheresis, donor-specific transfusion, and tolerogenic DC-based therapies in transplantation

Albert Ehrenstein Collection circa 1941, 1945

Correspondence with typewritten transcriptions dated between 1941 and 1945, addressed to Kürt Kläber, known also by his pseudonym Kurt Held. Undated poems, including one dedicated to his murdered brother, Otta. Photoreproduction of a Kokoschka drawing featuring a depiction of Albert Ehrenstein.Author, born 1886 in Vienna. Died 1950 in New York.The original German language inventory is available in the folder.Processed for digitizationSent for digitizationReturned from digitizationLinked to online manifestationdigitize

CD8alpha+ dendritic cells prime TCR-peptide-reactive regulatory CD4+FOXP3- T cells.

CD4(+) T cells with immune regulatory function can be either FOXP3(+) or FOXP3(-). We have previously shown that priming of naturally occurring TCR-peptide-reactive CD4(+)FOXP3(-) Treg specifically controls Vbeta8.2(+)CD4(+) T cells mediating EAE. However, the mechanism by which these Treg are primed to recognize their cognate antigenic determinant, which is derived from the TCRVbeta8.2-chain, is not known. In this study we show that APC derived from splenocytes of na\uefve mice are able to stimulate cloned CD4(+) Treg in the absence of exogenous antigen, and their stimulation capacity is augmented during EAE. Among the APC populations, DC were the most efficient in stimulating the Treg. Stimulation of CD4(+) Treg was dependent upon processing and presentation of TCR peptides from ingested Vbeta8.2TCR(+)CD4(+) T cells. Additionally, DC pulsed with TCR peptide or apoptotic Vbeta8.2(+) T cells were able to prime Treg in vivo and mediate protection from disease in a CD8-dependent fashion. These data highlight a novel mechanism for the priming of CD4(+) Treg by CD8alpha(+) DC and suggest a pathway that can be exploited to prime antigen-specific regulation of T-cell-mediated inflammatory disease