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Workshop A

Exploring the Use of Complement Inhibitors in Transplantation

9:00 am - 12:00 pm

The classical complement pathway is often activated within the first 9 weeks of transplantation due to early acute antibody-mediated rejection (AMR) being triggered by recipient donor-specific antibodies (DSAs) binding to donor human leukocyte antigens (HLAs). It has been shown that blocking the cleavage of C5 (thus preventing terminal complement activation) using Eculizumab lowers the incidence of acute AMR in highly sensitized recipients of living-donor kidney transplants compared with a historic control group. Just this one example displays the promise of complement inhibitors in transplantation. Understand how to properly design trials to display the efficacy of your complement inhibitor at this workshop.

Attend this workshop to:

• Hear lessons learned from the clinical design of trials in the transplant space
• Discuss data analysis from negative Eculizumab trials
• Discover that changing certain flaws in clinical trial design can lead to stunningly different results
• Debate patient stratification and its importance in clinical trial design

Robert Montgomery

Robert Montgomery
NYU Langone Transplant Institute

Robert A. Montgomery, MD, DPhil, FACS, is the Director of the NYU Langone Transplant Institute and a Professor of Surgery. He received his Doctor of Medicine with Honor from the University of Rochester School of Medicine. He received his Doctor of Philosophy from Balliol College, The University of Oxford, England in Molecular Immunology. Montgomery completed his general surgical training, multi-organ transplantation fellowship, and postdoctoral fellowship in Human Molecular Genetics at Johns Hopkins. For over a decade he served as the Chief of Transplant Surgery and the Director of the Comprehensive Transplant Center at Johns Hopkins.

Workshop B

The Inflammasomes: Linking Immunological Priming, Neuroinflammation, Complement Activation and the Development of Psychiatric Disorders

1:00 pm - 4:00 pm

We have proposed this workshop based on recent evidence which indicates that the exposure to multiple environmental stressors elicits proportionally stronger neuroinflammatory responses. This workshop will explore the neurochemistry underlying the nexus between immunological priming, the inflammasome complex, the complement system (CS), and microglia initiated neuroinflammation. Recent evidence suggests that immune system-based recognition of the pathogens or their pathogen associated molecular patterns (PAMPs) initiates the pro-inflammatory immune response required for the maintenance of homeostasis.

The overall goal of this workshop is to discuss how inflammasome mediated neuroinflammation contributes to the altered neurochemical signatures found in certain psychiatric disorders such as depression. Pattern recognition receptors (PRRs) including toll-like receptors (TLRs), complement receptors (CRs), and nucleotide-binding oligomerization domain and leucine-rich repeat-containing receptors (NLRs) of inflammasomes regulate both these processes of recognition of pathogens/PAMPs and their clearance have been implicated in novel therapeutic approaches in mental disorders. Moreover, recent evidence implicates the effect of the microbiome in TLRs mediated responses in the brain, and will be discussed in respect to new evidence of the role of inflammasome and depression. This workshop will include experts in the fields of neuroinflammation, inflammasome activation, complement system, and models of neuroimmunological priming in response to environmental stressors.

Attend this workshop to:

• The crosstalk between the CS and inflammasomes in the generation of pro-inflammatory immune response (eg C1q inactivation of NLRP3 inflammasome and CASP1 activation required for the release of IL-1b).

• The role of pathogen recognition by the CS and their interactions during various immunological processes including autophagy and innate immunity in response to stress induced psychological impairment.

• The enzymatic reactions that facilitate the transcription and activation of inflammasome complexes such as NLRP3 in the brain and how these complexes activate neuroinflammation, which can lead to synaptic maladaptation observed in
depression-like phenotypes.

• The expanding economic toll of psychiatric disorders that has fueled a demand to better understand the etiology of psychiatric disorders, and to develop new therapeutic approaches using rational drug design (including novel drug influencing the CS).

Given the recent focus on both the role inflammasomes play in catalyzing the activation of inflammatory cytokines as well as new therapeutics that target these complexes, now is the time to better understand the biochemical pathways involved in the activation of certain inflammasomes!

Giulio Pasinetti

Giulio Pasinetti
Icahn School of Medicine at Mount Sinai

Dr. Giulio Maria Pasinetti is the The Saunders Family Chair and Professor of Neurology, Neuroscience, and Geriatrics and Adult Development at the Ichan School of Medicine at Mount Sinai (ISMMS) in NY. He also serves as the Director of Basic and Biomedical Research in the Center for Geriatic Research and Training at the Bronx Veterans Affairs Medical Center. He is also the Director of the Center for Molecular Integrative Neuroresilience at the ISMMS. The Center’s goal is to understand the mechanisms of action through which novel therapeutics act against stressful events and to clarify the role of innate immunity in the gut/microbiome-brain axis at the genomic level in the promotion of cognitive and psychological resilience across the lifespan.