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Team / Porcelli

PorcelliSteven A. Porcelli MD

Professor, Department of Microbiology & Immunology
Professor, Department of Medicine (Rheumatology)
Chair, Department of Microbiology & Immunology
Murray and Evelyne Weinstock Chair in Microbiology & Immunology
Scientific Director, Flow Cytometry Core Facility
Tel: 718.430.3228
steven.porcelli [at] einstein.yu.edu

Dr. Porcelli’s laboratory focuses on the control of acquired immune responses by T cells, which are the master regulatory and key effector cells of host defense and immune tolerance. In broad terms, the research being pursued in the laboratory covers two interrelated areas. The first is to understand the role of regulatory T cells, with particular emphasis on the activities of a specialized T cell subset known as CD1d-restricted NKT cells. These T cells have the highly unusual property of responding to specific glycolipid antigens, which they recognize in combination with a specialized lipid antigen presenting molecule known as CD1d. The laboratory is studying the details of the cellular mechanisms that lead to the uptake and presentation of lipid antigens by CD1d, and is also using synthetic lipid antigens of NKT cells to determine how antigen structure controls the types of immune responses that are stimulated. The ability of lipid antigens that stimulate NKT cells to serve as adjuvants or immune modulators to control the outcome of disease processes is also being studied. The laboratory’s second major research area is the study of T cell responses against pathogenic microorganisms, especially Mycobacterium tuberculosis. Work in this area has recently led to significant progress in understanding how mycobacteria block effective host T cell responses, and this information is now being used to further the design of more effective vaccines for prevention of tuberculosis. A major near term goal of this research is to broaden the understanding of how organisms like M. tuberculosis successfully evade eradication by the immune system. The major long term goal is to create a genetically modified live attenuated M. tuberculosis strain that will be safe and effective as a vaccine against tuberculosis.

porcelli-aroraPooja Arora

Research Associate
718 430 3226/3227
pooja.arora [at] einstein.yu.edu

Natural Killer T cells (NKT cells) are an intriguing subset of T cells that recognize glycolipid antigens presented in the context of CD1d, an antigen presenting molecule similar to MHC class I.  Several studies have demonstrated that slight alterations in the lipid moiety can bias the NKT response towards either a pro- or anti-inflammatory type cytokine response. We have recently identified a single subset of dendritic cells, the DEC205+ CD8α+ dendritic cells, that efficiently internalize exogenous lipid antigens, accumulate iNKT stimulatory CD1d-loaded complexes and induce robust NKT responses. My current work focuses on identification of mechanism into how NKT cell responses are controlled and regulated by CD1d signaling in dendritic cells.


porcelli-ngTony W. Ng

Research Associate
718 430 3226/3227
tony.ng [at] einstein.yu.edu

I am interested in developing live-mycobacteria vaccines, especially against both Mycobacteria tuberculosis and HIV by using recombinant BCG vaccine strains that express HIV antigens, such as Gag and Env.  A cell-mediated immunity against Gag and a strong antibody response targeting Env are required to generate protective immune responses against HIV.  In order to modulate the desired type of immune responses, different glycolipids can be used to promote humoral or cellular immunity by skewing the production of Th1-like vs Th2-like cytokines from activated NKT cells.  Incorporating these glycolipid adjuvants onto the cell wall of rBCG vaccine strains resulted in their increased immunogenicity.  I am currently using glycolipid adjuvants to enhance immunogenicity on different attenuated auxotrophic rBCG vaccine strains that were made to express HIV antigens.  The balance of immunogenicity and attenuation are critical to the development of a successful tuberculosis/AIDS vaccine.


Neer_2Neeraj K. Saini

Research Associate
718 430 3226/3227
neeraj.saini [at] einstein.yu.edu

During the course of evolution M.tubculosis has evolved different mechanisms to survive inside the hostile environment of host cells which includes disruption of antigen processing and presentation. In order to identify the M.tuberculosis genes responsible for inhibition of MHC class II antigen-presentation, we have screened M.tuberculosis cosmid library and identify different cosmids involve which inhibits MHC class II antigen presentation. Currently I am working on the mechanism involved in the subversion of MHC Class II antigen presentation by one of the PE_PGRS family member which we identitied during our screen.

Carreno_2Leandro Carreno

Post-Doctoral Fellow
718 430 3226/3227
leandro.carreno [at] einstein.yu.edu

Invariant Natural Killer T cells (iNKT cells) are a specialized group of T lymphocytes which modulate many aspects of immune responses. They co-express an invariant T cell receptor (TCR) which recognizes glycolipid antigens bound to the CD1d molecule. Although mouse and human CD1d are relatively conserved, there are differences in the abundance and responses of human and mouse iNKT cells, which may correlate with differences in CD1d function. Thus, the study of iNKT cell responses and their role in disease models requires a more “humanized” model to enable more accurate translation of results to human therapy. My work is based on the characterization and use of a human CD1d knock-in mouse, which displays similar frequency and phenotype in their iNKT cells to humans. In order to improve MTB immunity, we have incorporated different glycolipid iNKT cell ligands into potential tuberculos (TB) vaccine candidates.  Our aim is to identify novel TB vaccines (with enchanced iNKT-cell activity) by using the human CD1d knock-in mouse.

porcelli-johnsonAlison J. Johnson

Research Fellow
718 430 3226/3227
alison.Johnson [at] einstein.yu.edu

My research focuses on defining the specificity of the CD4+ T cell response critical for protection afforded by IKEPLUS, a promising vaccine candidate in the defense against Mycobacterium tuberculosis (Mtb).  Utilizing a synthetic peptide library, a recombinant protein library, and libraries of CD4+ T cell hybridomas, the range of CD4+ T cell specificities generated upon immunization with IKEPLUS is being examined.  Results demonstrate that the CD4+ T cell response in IKEPLUS-immunized mice has multiple targets including components of the mycobacterial ribosome, representing novel specificities for protective responses against Mtb.  Further studies to more fully define the CD4+ T cell responses to ribosomal targets will inform the design of effective vaccines against Mtb.

porcelli-velayudhanShajo Kunnath

Research Fellow
718 430 3226/3227
shajo.kunnath [at] einstein.yu.edu

CD4+ T cells are critical for the protection against tuberculosis.  They protect against tuberculosis by secreting cytokines such as interferon gamma which activate effector cells such as macrophages.  I study characteristics of a type of CD4+ T cells that secrete interleukin-3 and its role in protection against tuberculosis.


porcelli-saavedraNoemi Alejandra, Saavedra

Research Fellow
718 430 3226/3227
alejandra.saavedra [at] einstein.yu.edu

Currently working in the generation of new immunotherapies against cancer in new murine models based in the incorporation of newly designed synthetic α-GC analogs into recombinant Listeria monocytogenes with multiple targeting of the well-defined human Tumor Associated antigens of melanoma, colon carcinoma, lung and breast.

 CYMERA_20151002_101437Shalu Sharma Kharkwal

Post-doctoral fellow
718 430 3226/3227
shalu.sharma [at] einstein.yu.edu

Invariant Natural Killer T cells (iNKT cells) are innate-like lymphocytes that recognize glycolipids presented by a non-classical MHC I like molecule CD1d.  α-Galactosylceramide (α-GC), which binds to CD1d to form complexes that are recognized by the antigen receptors of iNKT cells, is the most extensively studied activator of these cells. Many active analogues of the glycolipid have been identified which have immunotherapeutic and adjuvant effects in animal models, and studies of the structure-activity relationship of α-GC analogues have helped in design and selection of highly active iNKT cell agonists. However, generalized systemic activation of iNKT cells can lead to significant toxicity, and is also associated with the development of long-lived anergy or depletion of iNKT cells. My work mainly focuses on i) design and characterization of novel -galactosylceramide (α-GC) analogues and ii) designing and refining delivery methods for use in iNKT based immunotherapeutic agents and vaccines.

porcelli-johndrowChristopher T. Johndrow

Ph.D Student
718 430 3226/3227
christopher.johndrow [at] phd.einstein.yu.edu

Vaccination is by far the most effective means of controlling and eradicating infectious diseases. CD4 Helper T cells are critical to a vaccine’s efficacy. To improve current vaccine development we are investigating the ability of adjuvants, synthetic mimics of bacterial and viral signals recognized by the immune system, to shape the scale and character of immune responses. My work focuses on elucidating tissue specific mechanisms, specifically in the skin, that affect CD4 T cell response towards specific adjuvants with the ultimate goal of improving current vaccines and aiding the rational design of new vaccines.


porcelli-kennedySteven Kennedy

Ph.D Student
718 430 3226/3227
steven.kennedy [at] phd.einstein.yu.edu

My research focuses on understanding the differences in Tcell responses to fast growing and slow growing mycobacterium.  Using mycobacterium antigen libraries, we are able to probe a portion of the immune response to a fast growing mycobacterium, like M. smegmatis, or slow growers, such as M. bovis and M. tuberculosis. Analyzing the differences between the two Tcell responses to the antigen library can give insight into the inherent antigen shielding that the slow growing mycobacterium employ. Antigen shielding acts as a defense mechanism to hide immunogenic epitopes from the host’s immune system. Identifying the antigens that are hidden by the slow growing mycobacterium, will inform the development of new vaccine strategies to boost the efficacy of the currently available BCG vaccine against M. tuberculosis.