Image of Jain, Pooja

Pooja Jain, PhD


  • Department:Microbiology and Immunology
  • Education: PhD - Central Drug Research Institute (2001)
Research Overview

Research interests: Dendritic cells in chronic viral infections and neuroinflammatory diseases

Graduate students: Divya Sagar, Mohit Sehgal

Research staff: Rasha el Baz, MS, Anne Lamontagne, MS, Jasmine Shirazi


Dendritic cells (DCs) are the most potent antigen presenting cells and have long been recognized as key regulators of the immune system, linking both stimulatory and inhibitory components of normal immunity.  While DCs are well characterized with respect to primary and secondary immune responses, their unique role in coordinating central and peripheral tolerance is not fully delineated.  It is increasingly evident that the failure of DCs to maintain tolerance can lead to autoimmune and/or inflammatory diseases. For the last several years our efforts have been focused on investigating DC biology in the periphery with respect to chronic viral infections (i.e. HTLV-1 and HIV-1/HCV co-infection) and in the central nervous system with respect to autoimmunity (MS/EAE) and inflammation (glioblatoma multiforme). Currently three major projects are underway as follows:


Project 1: Quality and function of dendritic cells during HIV-1/HCV co-infection
Within the United States, approximately 1 million people are infected with HIV-1 and approximately 4 million people are infected with HCV. Globally, the prevalence of HIV-1/HCV co-infection is substantial with significant overlap in geographical areas and types of populations affected. Both HIV-1 and HCV share similar routes of transmission, where intravenous drug use (IDU) is possibly the main cause of high rates of HIV-1/HCV coinfection (up to 90% within the specific IDU population). Additionally, many individuals who received repetitive blood transfusions prior to mandatory HIV-1 and HCV screening were found to be co-infected. It is becoming increasingly evident that there is an acceleration of HCV-mediated liver disease as well as cirrhosis, liver failure, and hepatocellular carcinoma in HIV-infected individuals. HIV-1 has been shown to advance the course of HCV infection through increases in the rate of HCV viral persistence, RNA levels, progression to liver fibrosis and shortens survival in those with de-compensated cirrhosis. Similarly, infection with HCV has been shown to hinder immunological reconstitution after the initiation of antiretroviral therapy, and it contributes to liver toxicity in HIV-infected patients. However, little is known about the pathophysiology of HIV-1/HCV co-infection that results in advanced/accelerated hepatic diseases. It remains unknown whether immune activation or deficiencies due to HIV-1 infection are associated with the acceleration of liver disease in the co-infected individuals due to the lack of comprehensive immune profiling studies. Additionally, very limited serum proteomic profiling data has been available for the HCV mono-infected patients with no proteomics or glycoproteomics data reported so far from patients with HIV-1/HCV co-infection. To address these knowledge gaps, we are studying a well-defined cohort of HIV-1 and HCV mono- and co-infected individuals and monitor patients’ immunological, transcriptome, and proteome profiling in response to the interferon therapy. In addition, we are in the process of monitoring DC responses upon interferon/ribavirin treatment in non-responder and responder populations of co-infected individuals.

Dr. Pooja Jain's Luminex analyses of plasma cytokine and chemokine expression in HIV-1/HCV mono- and co-infected patients

Luminex analyses of plasma cytokine and chemokine expression in HIV-1/HCV mono- and co-infected patients. Left, the absolute concentrations of various cytokines and chemokines were normalized to healthy donor plasma and a pattern analysis was performed using a core developed software suite specific for Luminex® analysis. Results are presented as the mean plasma cytokine value for the sample (S) over the concentration from normal donor plasma (D) for that cytokine ({S/n)}/(D)) and arranged as an unsupervised distance clustered intensity plot. Right, the individual and median concentrations of various chemokines from HIV mono, HIV-1/HCV co-infected, and HCV mono-infected individuals (n=3 for each condition and are represented by diamond, circle and square symbols, respectively). The median value is represented by a bar.

Project 2: Dendritic cell trafficking into the CNS during neuroinflammation
The molecular mechanisms of how circulating DCs gain access to the central nervous system have not been investigated so far. Increase in immune cell infiltration across the blood-brain barrier (BBB) is influenced by chemokines. Monocyte chemotactic protein 1 (MCP-1) is one such potent chemoattractant known to be secreted by the astrocytes at the BBB. In order to understand the influence of MCP-1 on DC trafficking, both in vivo and in vitro imaging studies were undertaken in conjunction with transmigration assays. Near Infra-Red imaging of DCs’ CNS transmigration correlated with the severity of inflammation during experimental autoimmune encephalomyelitis (EAE). Histology confirmed MCP-1 presence in EAE lesions in concurrence with DCs emerging from perivascular spaces. DCs exhibited a better transmigration pattern as compared to T cells in BBB model studies. These observations correlated with those obtained by transwell imaging that has also indicated a paracellular versus transcellular pattern of migration by DCs and T cells, respectively. At the molecular level, MCP-1 seems to facilitate DC transmigration in an ERK1/2-dependent manner. These comprehensive continued studies provide state-of-the-art view of DCs within the CNS, elucidate their path across the BBB and highlight potential mechanisms involved in MCP-1-mediated DC trafficking that could be utilized to design both active (against glioblastoma) and passive (against MS) strategies to treat CNS-related disorders.

Dr. Pooja Jain's in vitro imaging showing movement of DCs across the endothelium in response to MCP-1


In vitro imaging showing movement of DCs across the endothelium in response to MCP-1. Human brain microvascular cells were grown to confluence on a collagen-coated PET membrane transwell inserts with 3 μm pores. Primary peripheral blood lymphocytes (PBLs) and monocyte-derived dendritic cells (MDDCs) were labeled with DAPI and added to the upper chamber of the transwell. At 30 minute after immune cell addition the transwells were washed, stained for ICAM-1 (green) or Caveolin-1 (red) and viewed at 100X to determine paracellular versus transcellular migration patterns.

Project 3: Mechanistic aspects of DC:T cell interaction during HTLV-1-associated cancer and neuroinflammatory disease. HTLV-1 is the etiologic agent of two immunologically distinct diseases; adult T cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), a chronic debilitating neuroinflammatory disease with similarities to MS. The humoral and cellular immune responses during HAM/TSP are directed to the HTLV-1 transactivator protein Tax that is oncogenic in nature. The molecular mimicry exhibited by anti-Tax antibodies to neuronal antigen (hnRNAP A1) and intense proliferation of chronically activated Tax-specific cytotoxic CD8+ T lymphocytes support the autoimmune nature of the disease. Therefore, HAM/TSP demonstrates a clear link between chronic viral infection and autoimmune disease of the CNS and allows for the direct comparison of the infecting agent with host antigens providing important insights into the pathogenesis of MS and other neuroinflammatory diseases. This project deals with defining the role of various DC subsets (myeloid and plasmacytoid) in regulating Tax-specific CTL response and associated neuroinflammation under three different experimental settings: in vitro using primary DC culture systems, ex vivo in HAM/TSP patients, and in vivo in a mouse model of neuroinflammation.  Ultimate goal of this project is to determine how DC biology can be harnessed to enhance or silence its function in a disease-specific manner. 

Dr. Pooja Jain's proposed model to explain the early interaction between HTLV-1 and dendritic cells

Proposed model to explain the early interaction between htlv-1 and dendritic cells.The model shown here attempts to explain some of the early steps in DC activation following infection with htlv-1. The upregulation of antiviral genes by the DCs and the viral mediated selective downregulation of key signaling molecules demonstrates the constant struggle for power between the dendritic cell and the virus.


Selected Publications

"Dendritic cells CNS recruitment correlates with disease severity in EAE via CCL2 chemotaxis at the blood-brain barrier through paracellular transmigration and ERK activation"
Sagar D, Lamontagne A, Foss C, Khan ZK, Pomper M, and P Jain
Journal of Neuroinflammation, in press, 2012.

"HTLV-1 Tax mediated downregulation 1 of miRNAs associated with chromatin remodeling factors in T cells with stably integrated viral promoter"
Rahman S, Quanna K, Khan Z.K, Pandya D, Wigdahl B. and Jain P
PLoS One, PLoS One, 7(4):e34490, 2012.

"Unique and differential protein signatures for HIV-1 and HCV mono-infection versus co-infection"
Boukli N.V, Shetty J,  Reis L, Cubano M, Ricaurte, P, Shah Z, Nickens A, Talal R, Philip and Jain P.
Clinical Proteomics, 9:11, 2012.

Mechanisms of dendritic cell trafficking across the blood-brain barrier"
Sagar, D., Foss, C., Baz, R., Martin, G., Khan, Z. K., and P. Jain.
Journal of Neuroimmune Pharmacology, 7:74-94, 2012.

"Co-transcriptional chromatin remodeling by small RNA species: A HTLV-1 perspective"
Aliya N, Rahman S,Khan Z.K, and Jain P.
Leukemia Research and Treatment, 2012: 1-15, 2012.

"Investigation of plasma biomarkers in HIV-1/HCV mono- and coinfected individuals by multiplex iTRAQ quantitative proteomics."
Shetty V,  Jain P, Z Nickens, Gomathinayagam S,  Mehta A, and  Philip R.
 A Journal of Integrative Biology, 15(10): 705-711, 2011.

"Dendritic cell mediated early immune responses are critical to controlling cell-free HTLV-1 infection."
Rahman S, Khan Z.K,  Wigdahl B, Jennings S,  Tangy F, and  Jain P.
Journal of Immunology, 186 (1): 390-402, 2011.

"Unique cytokine/chemokine signatures for HIV-1 and HCV mono- infection versus co-infection as determined by the Luminex® analyses."
Rahman S, Connolly J,  Manuel S,  Chehimi J, Montaner L, and  Jain P.
Journal of Clinical & Cellular Immunology, 2(1): 1000104-1000108, 2011. 

"A novel high throughput screening assay to identify inhibitor of HIV-1 gp120 interaction with DC-SIGN."
Tran T, El Baz R, Cuconati A, Arthos J, Jain P, and Z.K Khan.
Journal of Antivirals and Antiretrovirals, 3: 49-54, 2011. 

"The tug-of-war between dendritic cells and human chronic viruses"
Rahman S, Khan ZK, and Jain P
International Reviews of Immunology, in press, 2011.

"α4β1-integrin mediates the recruitment of immature dendritic cells across the blood-brain barrier during experimental autoimmune encephalomyelitis"
Jain P*, Coisne C, Enzmann G, Rottapel R, and Engelhardt B
Journal of Immunology, 184 (12): 7196-7206, 2010.

"Presentation of HTLV-1 Tax protein by dendritic cells: the underlying mechanism of HTLV-1 associated neuroinflammatory disease,"
Manuel S, . Schell T,  Acheampong E,  Rahman S,  Khan Z.K, and  Jain P.
Journal of Leukocyte Biology, 86: 1205-1216, 2009.

"DC-SIGN mediates cell-free infection and transmission of human T cell leukemia virus type 1."
Jain P, Manuel S, Khan Z.K., Ahuja J, and Wigdahl B.
Journal of Virology, 83: 10908-10921, 2009. 

"Identification of HTLV-1 Tax amino acid signals and cellular factors involved in secretion of the viral oncoprotein"
Jain P, Mostoller K, Flaig KE, Ahuja J, Alefantis T, Khan ZK, and Wigdahl B
Journal of Biological Chemistry, 282: 34581-34593, 2007.


"Isolation of bivittoside D from sea cucumber and activity thereof"
Lakshmi V, Pandey K, Saxena A, Madhusudanan KP, Srivastava MN, Khan ZK, Jain P, Gupta G, and Dhar JD (2004).
US patent no. U015092-8.

Book Chapter

Transgenic Animals in Research & Industry
Masih S, Jain P, and ZK Khan
Invited Chapter in the Edited Book, Elsevier Science Publications, in press, 2012.


Dr. Jain is a professor in the Department of Microbiology & Immunology at Drexel University College of Medicine.

Research Location

Department of Microbiology & Immunology
2900 W. Queen Lane
Philadelphia, PA 19129
Phone: 215-991-8393
Fax: 215-848-2271

Room number (office): G47A
Room number (lab): G69 & G74
Lab phone: 215-991-8364, 215-991-8381

Email Dr. Jain

Related Pages

Microbiology & Immunology

Biomedical Graduate Studies

Molecular Medicine & Infectious Disease

Pooja Jain Laboratory

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