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Day 2: Molecular Pattern Recognition Receptors Conference


Conference Proceeding CD Now Available
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Friday, April 12

8:00 am Morning Coffee

8:25 Chairperson’s Opening Remarks

Limin Shang, Ph.D., Head, Exploratory Science Section, Exploratory Science and Translational Medicine, NovImmune SA

 

TOLL-LIKE RECEPTORS 

8:30 Blockade of TLR4 Activation Represents a Promising Strategy in Diabetes

Limin Shang, Ph.D., Head, Exploratory Science Section, Exploratory Science and Translational Medicine, NovImmune SA

Dysregulation of Toll-like receptor 4 (TLR4) signaling via numerous ligands appears to play an underlying role in the pathogenesis of multiple inflammatory diseases. Thus, NI-0101, an anti-human TLR4 monoclonal antibody, was generated to have the capacity to interfere with LPS-induced signaling of TLR4 as well as other activators (i.e., endogenous or chemical ligands). To evaluate the role of TLR4 in beta islet cell biology, NI-0101 was shown to block human islet-induced immune cell activation. Furthermore, using an anti-mouse TLR4 mAb in vivo, blockade of TLR4 was efficient in protecting grafted islets from rejection in a mouse islet transplantation model as well as in murine models of diabetes. Taken together, these data promote blockade of TLR4 activation as a promising strategy in diseases associated with islet cell pathogenesis.

9:05 Therapeutic Antibody against Toll-Like Receptor 3 (TLR3) for the Treatment of Inflammation

Carine Paturel, Ph.D., Director, R&D, Innate Pharma

Innate Pharma is developing a therapeutic antibody against Toll-like Receptor 3 (TLR3), an immune checkpoint controlling inflammation. We have generated a panel of mouse anti-human TLR3 antibodies and humanization of several candidates is ongoing. In addition, Innate Pharma generated efficacy data in animal models of COPD, Colitis, Rheumatoid Arthritis and sepsis with surrogate rat anti-mouse TLR3.

9:40 Mechanisms of HIV-Mediated Inhibition of TLR4 Triggered Macrophage Activation

Souvenir Tachado, M.D., Assistant Professor, Medicine, Beth Israel Deaconess Medical Center

Alveolar macrophages (AM) express Toll-like receptors (TLRs) such TLR4, and we found significant derangement of TLR4-mediated activation of AM from asymptomatic HIV+ subjects. Furthermore, this derangement is specific, may represent AM reprogramming to an LPS-tolerant phenotype and is independent of HAART. In summary, HIV infection of AM results in targeted and specific impairment of macrophage TLR-mediated signaling pathways, impairing critical components of first line host defenses in the lungs.

10:15 Coffee Break with Exhibit and Poster Viewing

10:55 Development of a TLR7 Agonist to Treat Chronic Hepatitis B Virus (HBV) Infection

Simon Fletcher, Ph.D., Principal Scientist, Biology, Gilead Sciences

GS-9620 is a potent, selective agonist of human TLR7 being developed to treat chronic HBV (CHB). It has demonstrated promising antiviral activity in both the woodchuck and chimpanzee models of CHB, and single dose safety has been demonstrated in healthy volunteers. Data from these preclinical and clinical studies will be presented.

11:30 A Critical Role for Calcium Mobilization in Activation of the NLRP3 Inflammasome

Tiffany Horng, Ph.D., Assistant Professor, Department of Genetics and Complex Diseases, Harvard School of Public Health

The NLRP3 inflammasome mediates production of inflammatory mediators such as IL-1b and IL-18 and as such is implicated in a variety of inflammatory processes including infection, sepsis, autoinflammatory diseases and metabolic diseases. The proximal steps in NLRP3 inflammasome activation are not well understood. Here we elucidate a critical role for Ca2+ mobilization in activation of the NLRP3 inflammasome by multiple stimuli. We demonstrate that blocking Ca2+ mobilization inhibits assembly and activation of the NLRP3 inflammasome complex, and that Ca2+ signaling is pivotal in promoting mitochondrial damage. Our findings support a model for NLRP3 inflammasome activation by Ca2+-mediated mitochondrial damage.

12:05 Luncheon Presentation (Sponsorship Opportunity Available) or Lunch on Your Own 

1:45 Chairperson’s Remarks

Robert Hershberg, M.D., Ph.D., CEO, VentiRx Pharmaceuticals

1:50 TLR3-Expressing Tumor Parenchyma and Infiltrating NK Cells Promote Tumor Control in Hepatocellular Carcinoma

Valerie Chew, Ph.D., Research Scientist, Tumor Immunology (JPA) Lab, Singapore Immunology Network

Our work features the latest findings with convincing data about the role of TLR3 in controlling HCC. Our data is derived from in vitro, in vivo with HCC mouse models as well as from 172 HCC patients from Singapore, Hong Kong and Zurich.

2:25 The Significance of Toll-Like Receptor-9 in Triple Negative Breast Cancer

Katri Selander, M.D., Ph.D., Assistant Professor, Medicine, University of Alabama at Birmingham

TLR9 is an innate immunity DNA-receptor which is also widely expressed in various cancers. We demonstrated recently that low tumor TLR9 expression is a poor prognosis marker specifically in triple negative breast cancer. The aim of our continuing work is to characterize at the molecular level how the lack of tumor TLR9 promotes poor survival in these patients.

2:55 The Unique Biology and Clinical Relevance of Toll-Like Receptor 8

Robert Hershberg, M.D., Ph.D., CEO, VentiRx Pharmaceuticals

The biology of TLR8 is unique in humans given its expression on myeloid-derived dendritic cells, monocytes and NK cells. In addition, TLR8 can be targeted using small molecule agonists and antagonists. Preclinical and clinical data are emerging which highlight TLR8 as an important target in human disease.

3:30 POSTER SPOTLIGHT Inflammasomes Are Important Mediators of Bladder Inflammation

Francis M. Hughes, Jr., Ph.D., Medical University of South Carolina

4:05 End of Conference






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