< Brochure Homepage | Faculty Index | Pathology Homepage

Division of Immunology

Email pcat@jhmi.edu
Phone (410) 614-4174

Related Websites
Autoimmune Disease Research Center

Patrizio P. Caturegli, M.D.

Primary Appointment in Pathology; Joint Appointment in Molecular Microbiology & Immunology (BSPH)
Member, Graduate Program in Cellular and Molecular Medicine; Member, Graduate Program in Molecular Microbiology and Immunology (BSPH); Member, Graduate Program in Pathobiology

My laboratory studies autoimmune diseases of the endocrine glands, with particular focus on those affecting the thyroid and pituitary. The lab has shown that transgenic mice expressing interferon-gamma specifically in the thyroid gland develop a metaplastic transformation of the thyrocyte resembling the human Hürthle cell, a cell characteristically found in Hashimoto thyroiditis. This transformation depends upon the overexpression of the immunoproteasome, in particular of its LMP2 subunit. The lab is now evaluating the efficacy of new immunoproteasome inhibitors for the treatment of Hürthle cell lesions. In the pituitary model, studies have led to the development of a mouse model of autoimmune hypophysitis, a model that the lab is using to explore two aspects relevant for the human condition. The first one is the identification of the pituitary antigens recognized by the immune system in patients with hypophysitis. The second one is the recently reported association between hypophysitis and treatments used in patients with cancer to block T cell inhibitory signals, such as CTLA-4.

Lupi I, Raffaelli V, Di Cianni G, Caturegli P, Manetti L, Ciccarone AM, Bogazzi F, Mariotti S, Del Prato S, Martino E. Pituitary autoimmunity in patients with diabetes mellitus and other endocrine disorders. J Endocrinol Invest. 2013 Feb;36(2):127-31.

Bose V, Caturegli P, Conrad J, Omran W, Boor S, Giese A, Gutenberg A. Use of a clinicoradiological score to determine the presurgical diagnosis of autoimmune hypophysitis in a teenage girl. J Neurosurg Pediatr. 2013 Mar;11(3):335-9.

Caturegli P, De Remigis A, Chuang K, Dembele M, Iwama A, Iwama S. Hashimoto's thyroiditis: celebrating the centennial through the lens of the Johns Hopkins hospital surgical pathology records. Thyroid. 2013 Feb;23(2):142-50

Maleszewski JJ, Murray DL, Dispenzieri A, Grogan M, Pereira NL, Jenkins SM, Judge DP, Caturegli P, Vrana JA, Theis JD, Dogan A, Halushka MK. Relationship between monoclonal gammopathy and cardiac amyloid type. Cardiovasc Pathol. 2012 Oct 24.

Caturegli P, De Remigis A, Ferlito M, Landek-Salgado MA, Iwama S, Tzou SC, Ladenson PW. Anatabine ameliorates experimental autoimmune thyroiditis. Endocrinology. 2012 Sep;153(9):4580-7.

Iwama S, De Remigis A, Bishop JA, Kimura HJ, Caturegli P. Hürthle cells predict hypothyroidism in interferon-γ transgenic mice of different genetic backgrounds.Endocrinology. 2012 Aug;153(8):4059-66.

Email tamukele@jhmi.edu
Phone (410) 614-4441
Top of Page

Timothy K. Amukele, M.D., Ph.D.

Primary Appointment in Pathology

Dr. Amukele's research interests are twofold: clinical laboratories and chronic diseases in Sub-Saharan Africa (SSA). His goal is to drive the conversation about both issues by studying, documenting, and publicizing facts about them, such as;
  1. How many clinical labs are there?
  2. What is the quality of the work these labs do?
  3. How much do they charge for their tests?
  4. Are people getting value for the money being invested?
  5. What is the profile of individuals with kidney disease in SSA?

He has created a laboratory quality assurance that has been deployed in Eritrea, Bhutan, Uganda, and Malawi. He aims to create a system of laboratory quality assurance that produces measurable results in settings that do not have the regulatory buttress we have in the US.

He's interested in studying the etiology of chronic disease in Sub-Saharan Africa. Sub-Saharan Africa is especially attractive for elucidating disease mechanisms because it is the most genetically diverse region in the world, and reflects the biological and physical conditions where modern humans evolved. Current projects include a study of the spectrum of kidney disease in ambulatory patients in Kampala, Uganda.


Timothy K. Amukele, Lori J. Sokoll, Daniel Pepper, Dana P. Howard, Jeff Street. Impact of Unmanned Aerial System (Drone) Transport on Routine Chemistry, Hematology, and Coagulation Laboratory Results. Submitted

Lee Schroeder, Ali Elbireer, J. Brooks Jackson, Timothy K. Amukele. Laboratory Test Availability and Cost in Kampala, Uganda. Submitted

Robert Kalyesubula, Joseph Lunyera, Gyavira Makanga, Bruce Kirenga, Timothy K. Amukele. A 4-year survey of the spectrum of renal disease at the Mulago Hospital Renal Outpatient Clinic, Uganda Kidney International 2015 Mar; 87:663

Amukele TK, Lee Shroeder, J. Brooks Jackson, Ali Elbireer. Most clinical laboratory testing in kampala occurs in high-volume, high-quality laboratories or low-volume, low-quality laboratories: a tale of two cities. Am J Clin Pathol. 2015 Jan;143(1):50-6

Amukele TK, Lee Shroeder. Medical laboratories in sub-Saharan Africa that meet international quality standards. Schroeder LF, Amukele T. Am J Clin Pathol. 2014 Jun;141(6):791-5.

Ali Elbireer, Alex Opio, Hakim Sandagiua, Danstan Bagenda, J. Brooks Jackson, Timothy K. Amukele. The Good the Bad and the Unknown: Quality of Clinical Laboratories in Kampala, Uganda. PloS 2013 May 30 PMID: 23737993

Amukele TK, Soko D, Katundu P, Kamanga M, Sun J, Kumwenda NI, Taha TE. Vitamin D levels in Malawian infants from birth to 24 months. Arch Dis Child. 2012 Dec 7. PMID: 23220204

Amukele TK, Michael K, Hanes M, Miller RE, Jackson JB. External quality assurance performance of clinical research laboratories in sub-saharan Africa. Am J Clin Pathol. 2012 Nov;138(5):720-3. PMID: 23086773S

Email dcihako1@jhmi.edu
Phone (410) 614-4173

Related Websites
The Čiháková Laboratory

Top of Page

Daniela Cihakova, M.D., Ph.D.

Primary Appointment in Pathology
Member, Graduate Program in Pathobiology

In most of my research, I focus on the pathogenesis of myocarditis and its sequela, inflammatory dilated cardiomyopathy (DCMI). DCMI is among the most common causes of non-congenital, non-ischemic heart failure in people under the age of 40. It is also a frequent indication for heart transplantation. Despite the seriousness and prevalence of the inflammatory heart disease, there are still important gaps in our understanding of its mechanism. To help fill those gaps, we use a mouse model of myocarditis, called experimental autoimmune myocarditis (EAM).

I have been focusing on two main areas related to myocarditis. My first area of interest is the role of the inflammatory cytokines in myocarditis and DCMI. We have discovered that IL17A is critical for progression from myocarditis to DCMI while not being essential for myocarditis development (Baldeviano et al, 2010). We are currently investigating the mechanism of how IL-17A is driving DCMI. We have evidence that IL17A and cardiac resident cells interaction is critical for DCMI. My second area of interest is the role of the various inflammatory cells in myocarditis and how they contribute to the cardiac remodeling and DCMI. Clinically, different types of myocarditis are recognized based on the predominant infiltrating cell type such as giant cell myocarditis or eosinophilic necrotizing myocarditis. We have developed several models that reflect closely these clinical myocarditis entities. These models allow us to investigate the role of neutrophils, T cells, NK cells, myeloid cells and eosinophils and their contribution to cardiac inflammation and remodeling.

Beside myocarditis, my other interests include the pathogenic role of SSA/SSB antibodies in development of congenital complete heart block and the susceptibility to Candida infections in patients with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED).


Baldeviano GC, Barin JG, Talor MV, Srinivasan S, Bedja D, Zheng D, Gabrielson K, Iwakura Y, Rose NR, Čiháková D*. Interleukin-17A Is Dispensable for Myocarditis but Essential for the Progression to Dilated Cardiomyopathy. Circ Res. 2010; 106(10):1646-1655.

Barin JG, Christian Baldeviano G, Talor MV, Wu L, Ong S, Quader F, Chen P, Zheng D, Caturegli P, Rose NR, Čiháková D*. Macrophages participate in IL-17-mediated inflammation. Eur J Immunol. 2011; 42(3):726-736.

Barin JG, Talor MV, Baldeviano GB, Kimura M, Rose NR, Čiháková D*. Mechanisms of IFNg regulation of autoimmune myocarditis Experimental and Molecular Pathology 2010;89 (2):83-91.

Barin J, Rose NR, Čiháková D*. Macrophage diversity in cardiac inflammation. Immunobiology 2011; 217(5):468-75.

Čiháková D (Ed). Myocarditis. InTech Open Access Publisher, Rijeka, Croatia 2011. ISBN 978-953-307-289-0 http://www.intechopen.com/books/myocarditis

Čiháková D, Sharma RB, Fairweather D, Afanasyeva M, Rose NR. Animal models for autoimmune myocarditis and autoimmune thyroiditis. Methods Mol Med. 2004; 102:175-94.

Email bdetrick@jhmi.edu
Phone (410) 614-3286

Related Websites
Cytokine Laboratory

Top of Page

Barbara Detrick, Ph.D.

Director, Division of Immunology; Primary Appointment in Pathology; Joint Appointment in Molecular Microbiology & Immunology (BSPH)
Member, Graduate Program in Immunology; Member, Graduate Program in Molecular Microbiology and Immunology (BSPH)

My research interests bridge basic research and translational research in the clinical Immunology Laboratory. My primary research goal is to study immune responses in the eye. More specifically, my group has explored the retinal pigment epithelial (RPE) cell extensively as an important immunoregulatory and multifunctional ocular cell and tracked its role in ocular diseases. Over the last several years we have investigated innate immunity in the retina. RPE cells are key players in the first-line defense against invading organisms. TLRs are critical recognition receptors in the host defense against microbial pathogens and play pivotal role in innate immunity. Using real time PCR analysis, a variety of TLRs were discovered and shown to be up-regulated in human RPE cells. Moreover, TLR signaling in these cells generates several critical cytokines that impact a variety of pathologic processes within the eye. A key feature generated from these finding was that IFN-beta was shown to be immunosuppressive and inhibited selected experimental retinal diseases by down-regulating CXCL9 and ICAM-1 on retinal endothelial cells. These studies have now been extended to brain endothelial cells in experimental cerebral malaria. In addition, our laboratory has also developed a unique murine coronavirus model system, which identified for the first time how a virus can trigger a retinal degenerative process associated with an autoimmune component. Currently, this animal model has set the stage for developing standardized diagnostic methods to monitor retinal autoimmune reactivity in human retinal degenerative diseases.

More recently, my research efforts have also involved translational research and my laboratory is studying how cytokines regulate and modulate immune responses in selected immune based diseases. Specifically, we have been studying these molecules in vasculitis, infection and transplant rejection. Current efforts are focused on bringing together information concerning the role of cytokines in the development, progression and complications of these inflammatory conditions and in identifying their possible role as biomarkers of early inflammatory disease.


Hooks, J., Nagineni, C., Hooper, L., Hayashi, K., and Detrick, B.: IFN-beta Provides Immuno-protection in the Retina by Inhibiting ICAM-1 and CXCL9 in Retinal Pigment Epithelial Cells. J. Immunol. 2008. 180 (6) 3789-96.

Detrick, B. and Hooks, J.J.: Immune Regulation in the Retina. Immunologic Research, 2010. 47: 153-161.

Nagineni, C.N., Kommineni, V.K., William, A., Hooks, J.J., and Detrick, B.: IL-11 expression in retinal and corneal cells is regulated by interferon-gamma. Biochem Biophy Res Com. 2010. 391: 287-292.

Morrell, C.N., Srivastava, K., Swaim, A., Lee, M.T., Chen, J., Nagineni, C., Hooks, J.J., Detrick, B.: Beta interferon suppresses the development of experimental cerebral malaria. Infect Immun. 2011. 79 (4): 1750-8.

Nagineni, CN, Kommineni, VK, William A, Detrick B and Hooks, JJ. Regulation of VEGF expression in human retinal cells by cytokines: Implications for the role of inflammation in age-related macular degeneration. J Cell Physiol. 2012. 227: 116-126.

Allen JG, Weiss MT, Arnaoutakis GJ, Shah AS, and Detrick B. Perioperative recipient cytokine levels are associated with early graft dysfunction in human lung transplantation. Ann Thorac Surg. 2012. 93(6): 1843-1849.

Email ahamad@jhmi.edu
Phone (410) 614-3021

Related Websites
Hamad Lab

Top of Page

Abdel Rahim A. Hamad, B.V.Sc., Ph.D.

Primary Appointment in Pathology, Secondary Appointment in Medicine
Member, Graduate Program in Immunology; Member, Graduate Program in Pathobiology

Dr. Hamad, a veterinarian and immunologist by training, received his Ph.D. in immunology at the laboratories of Dr. John Kappler at the National Jewish Center and postdoctoral training with Drs. Drew Pardoll and Jonathan Schneck at the Johns Hopkins University School of Medicine. Dr. Hamad’s independent research is focused on investigating the role of the Fas death pathway in regulating T cell homeostasis, self-tolerance and organ-specific autoimmunity. Dr. Hamad’s group is particularly interested in tacking the question of why inactivating the Fas pathway prevents organ specific autoimmunity and leads to accumulation of a peculiar T cell type that lack both CD4 and CD8 coreceptors (referred to as double negative, DN, T cells). Because the Fas pathway is not required for host defense, understanding how it regulates self-tolerance can lead to novel therapies that do not cause immunosuppression. Our focus is on type 1 diabetes (T1D), Ischemic renal injury (IRI) and autoimmune lymphoproliferative disease (ALPS) using both clinical and animal models in collaboration with physicians and scientists here at Hopkins and the NIH.

Hamad AR, Arcara K, Uddin S, Donner T. 2012. The potential of Fas ligand (apoptosis-inducing molecule) as an unconventional therapeutic target in type 1 diabetes, Frontiers in immunology, 3:196

Gutfreund, R., and A. R. Hamad. 2011. Immunotherapy for Type 1 Diabetes: Necessity, Challenges and Unconventional Opportunities. Book chapter in: Type 1 Diabetes - Pathogenesis, Genetics and Immunotherapy. D. Wager, ed. INTECH, Janeza Trdine 9. 409-424.

Xiao, X., Mohamood, A.S., Uddin, S., Gutfreund, R., Nakata, S., Marshall, A., Kimura, H., Caturegli, P., Womer, K.L., Huang, Y., J. Schneck, Hideo Yagita and Abdel Rahim A. Hamad. 2011. Inhibition of Fas ligand in NOD mice unmasks a protective role for IL-10 against insulitis development. Am J Pathol. 179:725. PMID 21718680.

Ko, G.J., Jang, H.R., Huang, Y., Womer, K.L., Liu, M., Higbee, E., Xiao, Z., Yagita, H., Racusen, L., Hamad, A.R.A., and Rabb, H. 2011. Blocking fas ligand on leukocytes attenuates kidney ischemia-reperfusion injury. J Am Soc Nephrol 22, 732-742. PMID: 21436290

Abdel Rahim Hamad. 2010. Analysis of gene profile, steady state proliferation and apoptosis of double negative T cells in the periphery and gut epithelium provides new insights into the biological functions of the Fas pathway. Immunol. Res. 47:134-42. PMID 20066510

Mohamood AS, Bargatze D, Xiao Z, Jie C, Yagita H, Ruben D, Watson J, Chakravarti S, Schneck JP, Hamad ARA. 2008. Fas-mediated apoptosis regulates the composition of peripheral alpha/beta T cell repertoire by constitutively purging out double negative T cells. PLoS ONE 3:e3465. PMID 18941614

Email hlarman1@jhmi.edu
Phone (410) 614-6525

Related Websites
The Larman Laboratory

Top of Page

H. Benjamin Larman, Ph.D.

Primary Appointment in Pathology

The Larman laboratory develops and deploys new technologies to study the human immune system. Much of our work utilizes 'next generation' DNA sequencing to enable novel, massively parallel molecular assays. Examples of these technologies include:

- phage display of synthetic peptidome libraries for comprehensive, quantitative profiling of antibodies;

- ribosome display of ORFeome libraries for antigen discovery, protein-protein interaction studies, and drug target identification;

- ultrasensitive, multiplex RNA quantification techniques to monitor gene expression and detect microbes;

- pooled genetic screening to elucidate immune cell function and identify new therapeutic targets.

The laboratory uses these and other unbiased approaches to identify new opportunities for monitoring and manipulating immune responses.


Larman HB, Zhao Z, Laserson U, Li MZ, Ciccia A, Gakidis MAM, Church GM, Kesari S, LeProust EM, Solimini NL & Elledge SJ, “Autoantigen discovery with a synthetic human peptidome,” Nat. Biotech. 2011; 29(6): 535-41

Larman HB*, Salajegheh M*, Nazareno R, Lam T, Sauld J, Steen H, Kong SW, Pinkus JL, Amato AA, Elledge SJ & Greenberg SA, "Cytosolic 5′-nucleotidase 1A autoimmunity in sporadic inclusion body myositis," Ann. Neurol. 2012; 73(3): 408-18

Zhu J*, Larman HB*, Gao G, Somwar R, Zheng W, Laserson U, Ciccia A, Pavlova N, Church GM, Kesari S & Elledge SJ, "Protein interaction discovery using parallel analysis of translated ORFs (PLATO)," Nat. Biotech. 2013; 31(4): 331-4

Larman HB, Scott ER, Wogan M, Oliveira G, Torkamani A & Schultz PG, "Sensitive, multiplex and direct quantification of RNA sequences using a modified RASL assay," Nucleic Acids Res. 2014; 42(14): 9146-57.

Xu GJ, Kula T, Xu Q, Li MZ, Vernon SD, Ndung’ T, Ruxrungtham K, Sanchez J, Brander C, Chung R, O’Connor KC, Walker B, Larman HB, & Elledge SJ, “Comprehensive serological profiling of human populations using a synthetic human virome,” Science. 2015; 384(6239): aaa0698-1-9

Email ssadegh@jhmi.edu
Phone (410) 614-4931

Related Websites
Sadegh-Nasseri Laboratory

Top of Page

Scheherazade Sadegh-Nasseri, Ph.D.

Primary Appointment in Pathology; Secondary Appointment in Biophysics and Biophysical Chemistry
Member, Graduate Program in Immunology; Member, Graduate Program in Molecular & Computational Biophysics; Member, Graduate Program in Pathobiology

Two major interests of our lab include:

I. Understanding the molecular basis for the generation of ligands for presentation to CD4 T cells.

A fundamental step in the activation of T cells is the interaction of T cell antigen receptors on T cells with short fragments of foreign antigens bound to the proteins of Major Histocompatibility Complex, MHC, on antigen presenting cells such as Dendritic Cells. We have shown that binding of peptides to MHC class II molecules is a complex process and involves multiple kinetic and conformational intermediates (Sadegh-Nasseri, S and H M McConnell 1989, Sadegh-Nasseri, S, and R N Germain 1991, Sadegh-Nasseri, S, et al 1994, Natarajan, et al 1999a, Natarajan, et al 1999b, Sato et al 2000). We have learned that differences in conformation induced upon binding of peptides to MHC class II can be recognized by HLA-DM, an accessory molecule helping in the capture and selection of antigenic peptides during antigen processing (Chou and Sadegh-Nasseri 2000, Narayan et al 2007, Sadegh-Nasseri et al, 2012). We believe that the heterogeneity of peptide/MHC conformation is the basis for interaction with the accessory molecules involved in antigen processing and presentation such as HLA-DM and HLA-DO. To achieve these goals, we utilize different techniques in physical chemistry, biochemistry, nanotechnology, immunology, and molecular biology.

To understand the bases of immunodominance, we have developed a minimalist cell free antigen processing system composed of only purified protein components has been developed in our laboratory. In combination with mass spectrometry this system can identify physiologically relevant immunodominant epitopes of protein antigens (Hartman/Kim et al 2010). Using this unique system, we investigate contributions of different molecules in antigen processing to the selection of immunodominant epitopes.

II. Investigating the parameters that control differentiation and longevity of memory CD4 T cells.

The second main focus in the lab is to understand the engagement of T Cell Receptors by complexes of peptide/MHC II. This interaction is highly complex and results in a spectrum of responses in T cells that range from ignoring the antigenic stimulus to undergoing activation induced cell death. Somewhere in the middle of this range, T cells are positively stimulated to proliferate and make cytokines, or become tolerized and refractory to further antigenic stimulations.

We have established that low avidity engagement of T Cell Receptor by suboptimal numbers of peptide/MHC II complexes per Antigen Presenting Cell induces a reversible state of unresponsiveness in memory T cells (Korb et al., 1999, Mirshahidi et al., 2001, Mirshahidi et al., 2004, Dalai, et al, 2008, Dalai/Khoruzhenko 2011). These observations highlight the significance of antigen presenting cells (APCs) in regulation of memory T cell activation and dormancy. A major project in the lab is to dissect the genetic control of memory T cell differentiation and longevity over a long period of time in mice and to verify the findings in man.


Dalai SK, Khoruzhenko S, Drake CG, Jie CC, Sadegh-Nasseri S. Resolution of infection promotes a state of dormancy and long survival of CD4 memory T cells. 2011. IMMUNOLOGY AND CELL BIOLOGY, 89:870-81.

Hartman, IZ; Kim, A; Cotter, RJ, Walter K, Dalai SK, Boronina T, Griffith W, Lanar DE, Schwenk R, Krzych U, Cole RN, Sadegh-Nasseri S. A reductionist cell-free major histocompatibility complex class II antigen processing system identifies immunodominant epitopes. 2010. NATURE MEDICINE. 16:1333-40.

Narayan K, Chou CL, Kim A, Hartman IZ, Dalai S, Khoruzhenko S, Sadegh-Nasseri S. HLA-DM targets the hydrogen bond between the histidine at position 81 and peptide to dissociate HLA-DR–peptide complexes. 2007. NATURE IMMUNOLOGY, 8:92-100.

Mirshahidi S, Huang CT, Sadegh-Nasseri S. Anergy in peripheral memory CD4+ T cells induced by low avidity engagement of T cell receptor. 2001. JOURNAL OF EXPERIMENTAL MEDICINE. 194(6):719-31.

Chou C-L, Sadegh-Nasseri S. HLA-DM recognizes the flexible conformation of major histocompatibility complex class II. 2000. JOURNAL OF EXPERIMENTAL MEDICINE,192:1697-706.

Natarajan SK, Assadi M, Sadegh-Nasseri S. Stable peptide binding to MHC class II molecules is rapid and is determined by a receptive conformation shaped by prior association of low affinity peptides. 1999. JOURNAL OF IMMUNOLOGY,162: 4030-6

Email jschneck@jhmi.edu
Phone (410) 614-4589

Related Websites
Schneck Laboratory

Top of Page

Jonathan P. Schneck, M.D., Ph.D.

Primary Appointment in Pathology; Secondary Appointment in Medicine
Member, Graduate Program in Cellular and Molecular Medicine; Member, Graduate Program in Immunology; Member, Graduate Program in Pathobiology

Identification and characterization of T cell mediated immune responses and their immune signature are key elements to understanding the cellular immune response. A critical interaction that helps initiate and direct T cells is the interaction between a specific T cell receptor and a cognate antigen-Human Leukocyte Antigen (HLA) complex. My lab has had a long-term interest in characterizing and understanding this interaction using multiscale and multidimensional analyses of T cell responses. These studies have enhanced our insights into the basic biology of T cell response and ultimately may lead to development of novel therapeutic approaches.

A major focuse of the lab has been development of HLA-Ig based artificial Antigen Presenting Cell, aAPC, bead-based platform technologies used for expansion and analysis of antigen-specific murine and human T cells. This was has been supported by multiple NIH, DOD, and other grants. These studies provided the basis for the development of a “Lego-like” platform technology (Figure 1), which is an easy to assemble, reductionist, system in which different immunological signals can be attached to a central scaffold. We have used HLA-Ig based aAPC for: A-1 and A-3) T cell activation in vitro and in vivo, A-2) T cell diagnostic tool, B) depletion of unwanted T cells, and C) activation of NKT cells. Thus the potential applications of the HLA-Ig based aAPC include both positive and negative immunomodulatory effects on cellular immune responses in vitro and in vivo.


Perica K, Bieler JG, Edidin M, Schneck JP. Modulation of MHC binding by lateral association of TCR and coreceptor. Biophys J, 103(9):1890-8, 2013.

de Melo AB, Nascimento EJ, Braga-Neto U, Dhalia R, Silva AM, Oelke M, Schneck JP, Sidney J, Sette A, Montenegro SM, Marques ET. T-cell memory responses elicited by yellow fever vaccine are targeted to overlapping epitopes containing multiple HLA-1 and -II binding motifs. PLoS Negl Trop Dis, 7(1):Jan. 31, 2013 (Epub ahead of print).

Webb TJ, Li X, Giuntoli RL 2nd, Lopez PH, Heuser C, Schnaar RL, Tsuji M, Kurts C, OelkeM, Schneck JP. Molecular identification of GD3 as a suppressor of the innate immune response in ovarian cancer. Cancer Res, 72(15):3744-52, 2012.

Boyle S, Kolin DL, Bieler JG, Schneck JP, Wiseman PW, Edidin M. Quantum dot fluorescence characterizes the nanoscale organization of T cell receptors for antigen. Biophys J, 101(11):L57- 9, 2011.

Lee JB, Oelke M, Ramachandra L, Canaday DH, Schneck JP. Decline of influenza-specific CD8+ T cell repertoire in healthy geriatric donors. Immun Ageing, 8(6):4-11, 2011.

Xiao Z, Mohamood AS, Uddin S, Gutfreund R, Nakata C, Marshall S, Schneck JP, Yagita H, Hamad AR. Inhibition of Fax ligand in NOD mice unmasks a protective role for IL-10 against insulitis development. Am J Pathol, 179(2):725-32, 2011.


Copyright © 2017 Johns Hopkins University. All Rights Reserved