Kartika Padhan

Abstract Inflammatory bowel disease (IBD) causes chronic suffering from gastrointestinal inflammation and dysfunction that can progress to colon cancer1,2. The disease prevalence is increasing and there is an urgent need to better understand its pathogenic mechanisms to improve treatment.

Following the 1918 ‘Spanish Flu’ pandemic, outbreaks of emerging or re-emerging novel viral diseases, such as 1956 ‘Asian Flu’, 1968 ‘Hong Kong Flu’ and 2009 ‘Swine Flu’ have exerted great toll on human health [1]. For centuries, coronaviruses (CoV), the causative agents of common cold have been known to infect humans. Of the known six human CoV (HCoV), the severe acute respiratory syndrome CoV (SARS-CoV-1) originating in China caused the first CoV pandemic during 2002–2003 [2].

Abstract Early secretion of IL-12 by mouse dendritic cells (DCs) instructs T cells to make IFN-γ. However, only activated, but not naive T cells are able to license DCs for IL-12 production. We hypothesized that it might be due to different levels of CD40L expression on the surface of these cells, as CD40 signals are required for IL-12 production.