Cutting Edge: A Natural Antisense Transcript, AS-IL1α, Controls Inducible Transcription of the Proinflammatory Cytokine IL-1α

Dissecting the Role of a lncRNA and Involvement of Plasmodium Infections in the Innate Immune Response: A Dissertation

Natural antisense transcripts (NATs) are a class of long noncoding RNAs (lncRNAs) that are complementary to other protein-coding genes. Although thousands of NATs are encoded by mammalian genomes, their functions in innate immunity are unknown. Here, we identify and characterize a novel NAT, AS-IL1α that is partially complementary to IL-1α. Similar to IL-1α, AS-IL1α is expressed at low levels i...

Natural Antisense Transcript: A Concomitant Engagement with Protein-Coding Transcript

The vertebrate genome contains large spans of non-coding RNA, which for the most part were considered of little functional value to the organism. Recent studies have indicated that vertebrate genomes may have stored hidden secrets in this large span of non-coding RNA, which we refer to here as "Natural Antisense Transcripts (NATs)." NATs can be found in introns, exons, promoters, enhancers, int...

Use of Serum Levels of Proinflammatory Cytokine IL–1α in Chronic Hepatitis B

BACKGROUND The reasons for the chronic viral persistence of hepatitis B virus infection (HBV) are unknown, but are probably related to host immune factors. Cytokines play a significant role in immune defense. Interleukin-1 (IL-1) is a proinflammatory cytokine and some studies have demonstrated that IL-1 production was impaired in patients with chronic infections of hepatitis B virus, implying t...

Proinflammatory Cytokine Production Motif Is Selectively Required for Cutting Edge: A TLR9 Cytoplasmic Tyrosine

Cutting edge: IL-1α is a crucial danger signal triggering acute myocardial inflammation during myocardial infarction.

Myocardial infarction (MI) induces a sterile inflammatory response that contributes to adverse cardiac remodeling. The initiating mechanisms of this response remain incompletely defined. We found that necrotic cardiomyocytes released a heat-labile proinflammatory signal activating MAPKs and NF-κB in cardiac fibroblasts, with secondary production of cytokines. This response was abolished in Myd8...