Message from the Director
The CII is RECRUITING new faculty with expertise in a broad range of immunologic interests.. Early investigators who have first author publications in high-impact journals as well as current NIH funding are strongly encouraged to apply. In an effort to attract new and exceptional scientists, Rutgers has created a Chancellors Scholars Fund to help develop and support research programs of the highest quality faculty. Positions are full-time, tenure-track.
The CII at Rutgers New Jersey Medical School Cancer Center is a multidisciplinary and highly collaborative center with laboratories dedicated to researching allergies; chronic autoimmune diseases like Crohn's disease and ulcerative colitis; fungal pathogens; pain management; sepsis; toxoplasmosis; and Vitamin D. An exciting emerging area of investigation includes inflammatory skin conditions such as acne and rosacea.
Cores Facilities include Biostatistics Core; Center for Genome Informatics; Experimental Histology & Confocal Imaging Core; Flow Cytometry and Immunology Core Laboratory; Molecular Resource Facility; and the Transgenic Core Services among others.
The CII is an integral part of the Institute for Infectious and Inflammatory Diseases (i3D) a Chancellor level institute on the Rutgers Biomedical and Health Sciences (RBHS) campus. Infection and Inflammation has been selected as a signature area of strategic development and the i3D is already poised to become a national leader in this specialized area.
Administrator: Jennifer Yaney
New Faculty Profiles.............
Ricardo Rajsbaum, PhD
Robin Stephens, MS, PhD
Dr. Rajsbaum received his BSc from the National Autonomous University of Mexico (UNAM), in Mexico City, and his MSc from the Weizmann Institute of Science, Israel. He then received his Ph.D. from the National Institute for Medical Research, London, UK, in the laboratory of Anne O’Garra, and completed his postdoctoral training at Mount Sinai School of Medicine, New York in the laboratory of Adolfo Garcia-Sastre. Dr Rajsbaum joined the University of Texas Medical Branch (UTMB) as faculty in 2014 where he first developed his independent research program. While at UTMB Dr Rajsbaum’s lab made important contributions on the regulation of cytokine expression in immune cells, Pattern Recognition Receptor (TLR and RIG-I-like receptors) signaling, regulation and function of type-I Interferons (IFNs), and virus–host interactions, with a specific focus on the role of ubiquitin and TRIM E3-ubiquitin ligases in innate antiviral function. The lab identified novel mechanisms used by viruses to enhance their replication, by targeting host factors that can normally have antiviral functions. Dr. Rajsbaum's lab moved to Rutgers in May 2022 to develop the new Center for Virus-Host-Innate Immunity (CVHII). Current research is focused on the role of the E3-ubiquitin ligase TRIM6 during infections with highly pathogenic viruses (Ebola, Influenza, SARS-CoV-2), the role of the ubiquitin system in promoting replication of flaviviruses (Zika, dengue, West Nile), and SARS-CoV-2 replication, and the role of unanchored polyubiquitin chains in regulation of innate immune signaling. The lab uses biochemical and in vitro approaches to understand molecular mechanisms as well as animal models to study physiological relevance. The lab is a highly collaborative and inclusive environment and extremely values diversity career development.
Dr. Stephens grew up in Washington Heights in New York City and finished High School in Chicago before coming back for college at Cornell University and a Master’s at NYU School of Medicine. Dr. Stephens’ PhD in Immunology from Washington University, St. Louis was awarded for studies of Th1 and Th2 cell cooperation leading to asthma exacerbations, for example after viral infection. Postdoctoral studies at the National Institute for Medical Research in Mill Hill, London, UK, in the laboratory of Jean Langhorne, a pioneer of malaria immunology and pathology in animal models, led to the finding that in prolonged infection, Th1 responses can persist in a protective state. The overarching goal of the Stephenslab, founded initially in 2010 at the University of Texas Medical Branch, is to contribute to greater understanding of immunity to malaria and COVID-19 by defining mechanisms of adaptive immunity and pathology. There are 2 major themes in the lab: i) T cell activation, function and memory differentiation, including B cell help, cytokine production and immunometabolism, in malaria; and ii) mechanisms of inflammation and regulation of immunopathology in cerebral malaria and now in COVID-19. The lab largely uses in vivo approaches in animal models, immunofluorescence and flow cytometry to understand translationally relevant mechanisms of immunity and disease progression. We strive to maintain a vibrant, cooperative and inclusive scientific environment, with a strong focus on mentoring. Major recent findings being followed up now in the lab include: a chronic vaccine that prolongs malaria immunity; a critical role for microglia in protection from cerebral malaria; a role for eicosanoids in effector memory T cell formation; a role for Th2 cytokines in the regulation of COVID-19 (maSARS-CoV-2) lung pathology; a balance of cytokine production (IL-21, IFN-gamma) regulating CD4 T cells’ role in antibody production and parasite killing.
IN THE NEWS.............
Congratulations to Dr. Nicholas Bessman, Assistant Professor and Chancellor Scholar, for being selected to be one of only two Rutgers University nominees for the Searle Scholars Program.
In September 2022, Jianya Peng and Chandler Sy from Dr. Mark Siracusa’s lab published a paper in PNAS showing an important role for monocytes in maintaining central nervous system homeostasis following an intestinal parasite challenge. These studies represent an important contribution to the rapidly emerging field of neuroimmunology and suggest that infections occurring at distal sites can dramatically alter the host brain. These findings further showed that a previous infection may make the host less susceptible to subsequent forms of neuroinflammation. Given that neuroinflammation is associated with disorders such as Alzheimer’s and Parkinson’s disease, this work could inform the development of new therapeutic targets to treat neurogenerative conditions.
In August 2022, Darine El-Naccache published a paper in Cell Reports showing an important role for adenosine in triggering type 2 immune responses through binding the Adenosine A2b receptor expressed on intestinal epithelial cells. These studies were part of her Ph.D. dissertation research in Dr. Gause's laboratory, and the studies were done in collaboration with Dr. George Hasko at Columbia University. These findings further showed that the adenosine was derived from extracellular ATP and essentially functions as an endogenous danger signal likely triggered through tissue damage occurring as helminth parasites cross the intestinal barrier. The findings were highlighted in an article in Rutgers Today...more info
In August 2022, Dr. Aimee M. Beaulieu, Assistant Professor and Chancellor Scholar, Center for Immunity and Inflammation and Department of Microbiology, Biochemistry, & Molecular Genetics, and colleagues published a study in The Proceedings of the National Academy of Sciences demonstrating that the cytokine, IL-33, is a key regulator of pregnancy progression and type 2 immune responses at the maternal-fetal interface in mice. This collaborative study included researchers from Dr. Beaulieu’s team, and from the teams of Dr. Nataki Douglas in the Center for Immunity and Inflammation and Department of Obstetrics, Gynecology and Reproductive Health at Rutgers NJMS and Dr. Ripla Arora at Michigan State University. Dr. Nuriban Valero-Pacheco, the first author of the paper, demonstrated that pregnant mice lacking the Il33 gene exhibit diverse defects in key physiological and cellular processes in the uterine microenvironment that support pregnancy progression in mice, resulting in impaired fetal and placental development. These defects were associated with diminished Type 2 immune responses by uterine lymphocytes and myeloid cells at the maternal-fetal interface during early pregnancy. Ultimately, this work could inform future efforts to target IL-33 signaling to treat or prevent pregnancy disorders in women.
In April 2022, Dr. Karen Edelblum, Assistant Professor and Chancellor Scholar,Center for Immunity and Inflammation and Department of Pathology, Immunology & Laboratory Medicine, and colleagues published a report in Mucosal Immunology identifying a novel γδ IEL hyperproliferative phenotype that arises early in life in mice. Dr. Luo Jia in collaboration with Dr. Guojun Wu, found that thisγδ IEL phenotypewas attributed totwo guilds of small intestinal or fecal bacteria represented by 12 amplicon sequence variants (ASV) that are strongly associated with γδ IEL expansion. Moreover, the hyperproliferative and hypermotileγδ IEL phenotype could be transferred via the microbiota to other mice. Based on previous studies showing that patients with active Crohn's disease exhibit areduced frequency of intestinalγδ IELs, these findings suggest that microbiota-derived signals may be useful in amplifyingγδ IEL number or surveillance function to reinforce the intestinal epithelial barrier and prevent disease relapse.
Dr. William Gause and Dr. Patricia Fitzgerald-Bocarsly, were recently named Fellows of the American Association for the Advancement of Science...more