Postdoctoral Fellow And Instructor Resume Example

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Jessica Claire
  • Montgomery Street, San Francisco, CA 94105
  • H: (555) 432-1000
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  • Date of Birth:
  • India:
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  • single:
Professional Overview
I am a multidisciplinary and resourceful scientist specializing in innate immunity and inflammation. My general research focuses on understanding the impact of the innate immune response during chronic inflammatory diseases. I have utilized in vitro or ex vivo molecular biology, biochemistry and cell biology to understand cellular immune responses and in vivo mouse models to help translate this information to complex disease models. My aim is to lead scientific efforts to target intractable diseases and use immune-modulation as a basis of efficacious therapies.
Core Qualifications
  • Research in autoimmunity 
  • ​Innate immunity
  • Scientific writing (Grants and Lay abstracts)
  • Group Instruction
  • Ad hoc Peer reviewing
  • Training of personnel and management of funding and resources
  • Initiated an entirely new area of research in the lab which was not my expertise.
  • Composed research plan, identified appropriate models of disease, defined long-term direction and obtained significant funding to execute this research plan.
  • Initiated and maintained fruitful collaborations with leaders in the fields of autoimmunity (Ann Rothstein, Mark Shlomchik, Michael Cancro, John Hartley and John Cambier).
  • Successfully integrated pre-doctoral and post-doctoral training to fully assess the contribution of cellular pathways to autoimmunity.
  • This work has resulted in the training of peers, students and technicians in the scientific process of question identification and execution.
  • This project required that I closely manage available resources, funding and time. 
  • ​My fruitful execution of this work has led to the publication of this study in an impactful journal and is supplemented by additional published studies on other models of disease.
: , Expected in Present
Instructor | U. Mass. Medical School - Worcester, MA
: PhD (Cell Biology and Molecular Genetics), Expected in
U. Maryland - College Park, MD
PhD (Cell Biology and Molecular Genetics) Jessica Claire | | Autoimmnunity. Inflammation. Innate Immunity. Infectious Diseases. Malaria.
MS: Microbiology and Biotechnology, Expected in 2002
Univ. of Mumbai - Mumbai,
Microbiology and Biotechnology
BS: Microbiology and Biotechnology, Expected in 2001
R. Ruia College, Univ. of Mumbai - ,
Microbiology and Biotechnology Publications All of my publications can be viewed at: ection= descending
 B-cell signaling and cytoskeletal rearrangements are critical aspects of B-cell mediated antigen recognition and response. The coordination of these events at the cell surface was the focus of my doctoral work. My doctoral work utilized two models of immunodeficiencies Xid (Btk) and Wasp (WASP) deficiency to understand the crosstalk between key components of B-cell receptor (BCR) signaling and cytoskeletal machinery for productive and efficient antigen processing and presentation. 
  • To understand if BCR signaling modulates cytoskeletal changes and BCR internalization, I used measurements of signaling (Ca2+ flux, phospho-Flow, etc.) tandemly with BCR internalization assays using pulse-chase stimulations.
  • By labelling the cytoskeleton with G-actin coupled fluors I could visualize the dynamic nature of actin cytoskeletal changes proximal to the BCR.
  • My work identified the key upstream players in both the signaling and cytoskeletal machinery and highlighted the cooperativity between BCR internalization and signaling.
Postdoctoral Fellow and Instructor, 2008 to Current
U. Mass. Medical School City, STATE,


Plasmodium species are the protozoan parasite responsible for malaria. Symptoms of malaria include fever, malaise, chills, and body aches, which suggest a highly pro-inflammatory state. I investigated the molecular components of the type I IFN and inflammasome pathways that contributed to inflammation during malaria using both in vitro and in vivo mouse model of infection.

  • Using knockout mouse models, determined the signaling components that contributed to the pathology and eventually to mortality during malaria.
  • Optimized and adopted new infection protocols utilizing Plasmodium-infected RBCs setting the stage for future investigations.  
  • This project was spear-headed by me and my work resulted in one high impact first author paper and several projects that stemmed from these initial studies. 


Cytosolic DNA sensing pathways are now increasingly implicated in myriad infectious and autoimmune diseases.The identification of bonafide sensors and contributors to this response has been a particular focus of mine. My largest contributions to this field are as yet unpublished works identifying novel players in cytosolic DNA sensing. Much of my work on characterizing DNA-sensing pathways stemmed from the identification of a unique AT-rich motif ubiquitous in the Pf genome that are also over- represented in the genomes of DNA viruses, bacteria and retroelement-derived repeats in mammals. I have since used this motif in a mass-spectrometry based proteomic screen to identify two novel players in the cytosolic DNA-sensing pathway.

  • To identify a cohort of novel nucleic acid binding proteins, I designed a proteomic (LC/MS) approach which has led to the discovery of several novel candidates that play unique roles in nucleic acid sensing.
  • Established key domains in candidates required for DNA binding by using alphascreen assays. 
  • Using proteomic softwares and bioinformatics I was able to correctly postulate the cellular localization, conservation and predicted interaction partners of the shortlisted candidates.
  • By employing a variety of gene silencing techniques (siRNA, shRNA and CRISPR/Cas9) and gene-overexpression (dCas9/SAM, retroviral overexpression) I was able to generate all the tools necessary for initial characterization and description of candidate nucleic acid binding proteins.
  • To characterize these uncharacterized genes, I designed cloning strategies and primers for qRT-PCR.
  • The value of these DNA-sensing proteins was assessed to several microbial pathogens including DNA and RNA viruses, gram negative and positive bacteria and Plasmodium spp. 
  • By characterizing the cell-death pathways including apoptosis, necroptosis as well as inflammasome dependent stimuli induced by microbes, I was able to fully evaluate the contribution of these proteins to the innate immune profile.
  • I have been able to understand the contribution of these candidates to the innate immune transcriptome by generating RNA-seq libraries of primary human DCs and murine BMDMs in response to viruses and intracellular nucleic acids. 
  • To fully assess the molecular mechanisms employed by these proteins to alter immune gene transcription, I am currently optimizing transcription factor and histone chromatin immunoprecipitation (ChIP). 


The hallmark of autoimmunity is the dramatic loss of immune homeostasis. My research focused on understanding the contribution of the cytosolic DNA-sensing pathway in modulating autoimmunity.

  • My studies are the first to show the existence of a critical regulatory loop between nucleic acid sensing receptors in the endosome and cytosol during chronic inflammation and autoimmunity.
  • By generating and studying multiple models of autoimmunity I have gained a unique perspective on understanding the distinct contribution of the different innate pathways to autoimmunity.
  • These studies involved in vivo characterization of diseased autoimmune mice (lupus nephritis, gross immuno-pathology), FACS based identification of rare subsets of cells, in situ staining of tissue-associated molecules and cells and led to an identification of a role for myeloid lineage cells in autoimmunity - a concept that is largely ignored by the community.
  • To gain a mechanistic handle on how these innate immune pathways cooperate during inflammation, I then assessed the involvement of cellular metabolic and homeostatic pathways such as autophagy, mTOR signaling, lysosomal biogenesis and ER stress.
  • My work resulted in 1 first-author publication, several second and third author papers and 2 review articles.


Age-induced changes in immune-homeostasis often result in chronic syndromes associated with age. Osteoporosis/Osteopenia, are hallmarks of age-induced changes, whereby a catabolic shift in bone metabolism has deleterious effects on the host. Intriguingly, modulators of bone homeostasis include osteoblasts (OB) derived from mesenchymal precursors and osteoclasts (OC) derived from myeloid progenitors. OCs utilize immune mechanisms for osteoclastogenic activities and thus, many pathways operative in myeloid cells have direct impact on bone metabolism. My research is focused on understanding the contribution of cytosolic DNA-sensing pathways to bone metabolism with age.

  • To fully assess the role of cytosolic DNA sensing pathways in bone homeostasis, I carefully characterized the long bone phenotypes in various strains using microcomputed tomography (microCT) to assess the rate of bone-deposition with age and noted that with age some strains are likely to lose bone faster.
  • To assess transcriptional profile of key cell types during these processes, I designed and utilized a unique nanostring codeset to gauge changes in key bone morphogenetic factors. 
  • To evaluate the cellular contribution to changes in bone remodeling, I have studied osteoblastogenesis and osteoclastogenesis and identified cell-specific changes in activity, pinpointed an endogenous DNA ligand which drives this process and further identified the downstream signaling pathway that potentiate cellular signaling leading to bone loss.
Fellowships and Awards
2013                Travel Award for American Association of Immunology Conference, Hawaii
2012                Travel Award for Keystone Symposia for Innate Immunity, Keystone, CO
2011                Best Poster Award Symposia for Innate Immunity, Toll 2011, Lago di Garda, Italy.
2010                Conference Assistant D3 Innate Immunity Symposia, Keystone Symposia, Dublin, Ireland.
2008                Distinguished Graduate Student Award, Graduate School, UMD
2007                Student Author Travel Award, Dept. of CBMG, UMD
2007                Jacob K. Goldhaber Travel Award, UMD
2002-2004       Graduate Flagship Fellowship, Dept. of CBMG, UMD
2002                Gold Medal, Certificate of Distinction and Monetary Scholarship, University of Mumbai, India
2001                Certificate of Distinction and Monetary Scholarship, Faculty of Science, R. Ruia College, University of Mumbai, India  
All of my publications can be viewed at: descending  
1. Claire S, Marshak-Rothstein A. Nucleic Acid Sensing Receptors - Rheostats of Autoimmunity and Autoinflammation. Oct 15;195(8):3507-12. Review. PMID: 26432899
2. Claire S, Campbell AM, Chan J, Schattgen SA, Orlowski GM, Nayar R, Huyler AH, Nündel K, Mohan C, Berg LJ, Shlomchik MJ, Marshak-Rothstein A, Fitzgerald KA. Suppression of systemic autoimmunity by the innate immune adaptor STING. Proc Natl Acad Sci USA. 2015 Feb 17;112(7):E710-7. Epub 2015 Feb 2. PMID: 25646421
3. Claire S, Deoliveira RB, Kalantari P, Parroche P, Goutagny N, Jiang Z, Chan J, Bartholomeu DC, Lauw F, Hall JP, Barber GN, Gazzinelli RT, Fitzgerald KA, Golenbock DT. 2011. Innate Immune Recognition of an AT-Rich Stem-Loop DNA Motif in the Plasmodium falciparum Genome. Immunity. Aug 26;35(2):194-207. Epub 2011 Aug 4. PMID:21820332
4. Unterholzner L, Keating SE, Baran M, Horan KA, Jensen SB, Claire S, Sirois C, Jin T, Xiao T, Fitzgerald KA, Paludan SR, Bowie AG. 2010. IFI16 is a novel innate immune sensor for cytoplasmic DNA. Nat Immunol. 2010 Nov;11(11):997-1004. Epub 2010 Oct 3. PMID: 20890285
5. Rathinam VA, Jiang Z, Waggoner SN, Claire S, Cole LE, Waggoner L, Vanaja SK, Monks BG, Ganesan S, Latz E, Hornung V, Vogel SN, Szomolanyi-Tsuda E, Fitzgerald KA, 2010. The AIM2 inflammasome is essential for host defense against cytosolic bacteria and DNA viruses. Nat Immunol. 11(5): 395-402. PMID: 20351692
6. Claire S, Orlowski GM, Song W. 2009. Btk regulates B-cell receptor-mediated antigen processing and presentation by controlling the actin dynamics of B-cells", J Immunol. 182(1):329-39. PMID: 19109164
1. Orlowski G.M., Claire S, Colbert J.D., Robertson S.A., Bogyo M., Rock K.L. The role of multiple cathepsins and mitochondrial membrane potential in particle induced cell death and IL- 1b production. 2015 (Submitted)
2. Baum R, Claire S, Organ J.M., Burr D.B., Hornung V, Marshak-Rothstein A, Fitzgerald KA, Gravallese E.M. Accrual of DNA promotes bone formation that is abrogated by STING deficiency. 2015 (Submitted)
3. Claire S, Baum R, Marshak-Rothstein A, Fitzgerald KA, Gravallese E.M. STING modulates aging associated bone homeostasis through recognition of endogenous retroelements. (In preparation).
2014                Invited talk at Alliance for Lupus Annual Investigators Meeting, NYC
2013                Invited talk for AAI May, Hawaii
2011                Invited talk at CFAR AIDS day
2010                Invited talk at Keystone D3 “Innate Immunity links to Adaptive Immunity”, Dublin, Ireland
Memberships/Scholarly Societies
Member, American Association for the Advancement of Science (2004-2005)
Member, American Society of Cell Biology (2004-2008)
Member, American Association of Immunology (2012-present)
Live cell confocal microscopy, mammalian cell culture (primary and cell lines, human and murine), alphascreens, multi-color FACS, ELISA, molecular biology (immunoprecipitation, western blotting, qRT-PCR, cloning, nanostring analysis), RNA-seq library preparation, In vivo models of autoimmunity and infections, Training students, technicians and postdoctoral fellows.

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Resume Overview

School Attended
  • Instructor | U. Mass. Medical School
  • U. Maryland
  • Univ. of Mumbai
  • R. Ruia College, Univ. of Mumbai
Job Titles Held:
  • Postdoctoral Fellow and Instructor
  • MS
  • BS