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Evaluation Of The Contribution Of Multiple Damps And Damp Receptors In Cell Death-Induced Sterile Inflammatory Responses, Hiroshi Kataoka, Hajime Kono, Zubin Patel, Kenneth L. Rock 2014 University of Massachusetts Medical School

Evaluation Of The Contribution Of Multiple Damps And Damp Receptors In Cell Death-Induced Sterile Inflammatory Responses, Hiroshi Kataoka, Hajime Kono, Zubin Patel, Kenneth L. Rock

Open Access Articles

When cells die by necrosis in vivo they stimulate an inflammatory response. It is thought that this response is triggered when the injured cells expose proinflammatory molecules, collectively referred to as damage associated molecular patterns (DAMPs), which are recognized by cells or soluble molecules of the innate or adaptive immune system. Several putative DAMPs and/or their receptors have been identified, but whether and how much they participate in responses in vivo is incompletely understood, and they have not previously been compared side-by-side in the same models. This study focuses on evaluating the contribution of multiple mechanisms that have been ...


The Hunt For Protective Correlates Of Immunity To Plasmodium Falciparum Malaria, Ann M. Moormann, V. Ann Stewart 2014 University of Massachusetts Medical School

The Hunt For Protective Correlates Of Immunity To Plasmodium Falciparum Malaria, Ann M. Moormann, V. Ann Stewart

Open Access Articles

Determining an immunologic correlate of protection against Plasmodium falciparum malaria has been the holy grail of natural infection studies, and sought after as an endpoint for malaria vaccine trials. An in vitro assay that provides an accurate and precise assessment of protective immunity to malaria would make smaller, short-duration studies feasible, rather than the currently powered study designs that use morbidity or mortality as outcomes. Such a biomarker would be especially desirable in situations where malaria control measures that result in decreases in clinical endpoints and putatively waning protective immunity have been implemented. In an article published in BMC Medicine ...


Tlr4 Activation Induces Il-1ss Release Via An Ipaf Dependent But Caspase 1/11/8 Independent Pathway In The Lung, Suffwan Eltom, Maria G. Belvisi, Liang Yew-Booth, Bilel Dekkak, Sarah A. Maher, Eric D. Dubuis, Victoria Jones, Kate A. Fitzgerald, Mark A. Birrell 2014 Imperial College London

Tlr4 Activation Induces Il-1ss Release Via An Ipaf Dependent But Caspase 1/11/8 Independent Pathway In The Lung, Suffwan Eltom, Maria G. Belvisi, Liang Yew-Booth, Bilel Dekkak, Sarah A. Maher, Eric D. Dubuis, Victoria Jones, Kate A. Fitzgerald, Mark A. Birrell

Open Access Articles

Background: The IL-1 family of cytokines is known to play an important role in inflammation therefore understanding the mechanism by which they are produced is paramount. Despite the recent plethora of publications dedicated to the study of these cytokines, the mechanism by which they are produced in the airway following endotoxin, Lipopolysaccharide (LPS), exposure is currently unclear. The aim was to determine the mechanism by which the IL-1 cytokines are produced after LPS inhaled challenge.

Methods:Mice were challenged with aerosolised LPS, and lung tissue and bronchiolar lavage fluid (BALF) collected. Targets were measured at the mRNA and protein level ...


Induction Of Il-12 Production In Human Peripheral Monocytes By Trypanosoma Cruzi Is Mediated By Glycosylphosphatidylinositol-Anchored Mucin-Like Glycoproteins And Potentiated By Ifn- Gamma And Cd40-Cd40l Interactions, Lucia Cristina Abel Jamli, Ludmila Rodrigues Ferreira Pinto, Isabela Cunha Navarro, Monique Andrade Baron, Jorge Kalil, Ricardo T. Gazzinelli, Luiz Vicente Rizzo, Edecio Cunha-Neto 2014 University of Sao Paulo

Induction Of Il-12 Production In Human Peripheral Monocytes By Trypanosoma Cruzi Is Mediated By Glycosylphosphatidylinositol-Anchored Mucin-Like Glycoproteins And Potentiated By Ifn- Gamma And Cd40-Cd40l Interactions, Lucia Cristina Abel Jamli, Ludmila Rodrigues Ferreira Pinto, Isabela Cunha Navarro, Monique Andrade Baron, Jorge Kalil, Ricardo T. Gazzinelli, Luiz Vicente Rizzo, Edecio Cunha-Neto

Open Access Articles

Chagas disease, caused by the protozoan parasite Trypanosoma cruzi (T. cruzi), is characterized by immunopathology driven by IFN-gamma secreting Th1-like T cells. T. cruzi has a thick coat of mucin-like glycoproteins covering its surface, which plays an important role in parasite invasion and host immunomodulation. It has been extensively described that T. cruzi or its products-like GPI anchors isolated from GPI-anchored mucins from the trypomastigote life cycle stage (tGPI-mucins)-are potent inducers of proinflammatory responses (i.e., cytokines and NO production) by IFN-gamma primed murine macrophages. However, little is known about whether T. cruzi or GPI-mucins exert a similar action ...


Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death: A Dissertation, Dan Weng 2014 University of Massachusetts Medical School

Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death: A Dissertation, Dan Weng

GSBS Dissertations and Theses

Yersinia pestis (Y. pestis), as the causative agent of plague, has caused deaths estimated to more than 200 million people in three historical plague pandemics, including the infamous Black Death in medieval Europe. Although infection with Yersinia pestis can mostly be limited by antibiotics and only 2000-5000 cases are observed worldwide each year, this bacterium is still a concern for bioterrorism and recognized as a category A select agent by the Centers for Disease Control and Prevention (CDC). The investigation into the host-pathogen interactions during Y. pestis infection is important to advance and broaden our knowledge about plague pathogenesis for ...


Fty720 (Fingolimod) Provides Insight Into The Molecular Mechanisms Of Multiple Sclerosis, Madelyn Elizabeth Crawford 2014 University of Tennessee, Knoxville

Fty720 (Fingolimod) Provides Insight Into The Molecular Mechanisms Of Multiple Sclerosis, Madelyn Elizabeth Crawford

Pursuit - The Journal of Undergraduate Research at the University of Tennessee

Multiple sclerosis (MS) is a neurodegenerative disorder caused by a prolonged immune- mediated inflammatory response that targets myelin. Nearly all of the drugs approved for the treatment of MS are general immunosuppressants or only function in symptom management. The oral medication fingolimod, however, is reported to have direct therapeutic effects on cells of the central nervous system in addition to immunomodulatory functions. Fingolimod is known to interact with sphingosine-1-phosphate (S1P) receptors, and the most widely- accepted theory for its mechanism of action is functional antagonism of the receptor. This review examines significant neuromodulatory effects achieved by functional antagonism of the ...


High-Throughput Sequencing Analysis Of Post-Liver Transplantation Hcv E2 Glycoprotein Evolution In The Presence And Absence Of Neutralizing Monoclonal Antibody, Gregory J. Babcock, Sowmya Iyer, Heidi L. Smith, Yan Wang, Kirk Rowley, Donna M. Ambrosino, Phillip D. Zamore, Brian G. Pierce, Deborah C. Molrine, Zhiping Weng 2014 University of Massachusetts Medical School Worcester

High-Throughput Sequencing Analysis Of Post-Liver Transplantation Hcv E2 Glycoprotein Evolution In The Presence And Absence Of Neutralizing Monoclonal Antibody, Gregory J. Babcock, Sowmya Iyer, Heidi L. Smith, Yan Wang, Kirk Rowley, Donna M. Ambrosino, Phillip D. Zamore, Brian G. Pierce, Deborah C. Molrine, Zhiping Weng

University of Massachusetts Medical School Faculty Publications

Chronic hepatitis C virus (HCV) infection is the most common cause of end-stage liver disease, often leading to liver transplantation, in which case circulating virions typically infect the transplanted liver within hours and viral concentrations can quickly exceed pre-transplant levels. MBL-HCV1 is a fully human monoclonal antibody recognizing a linear epitope of the HCV E2 envelope glycoprotein (amino acids 412-423). The ability of MBL-HCV1 to prevent HCV recurrence after liver transplantation was investigated in a phase 2 randomized clinical trial evaluating six MBL-HCV1-treated subjects and five placebo-treated subjects. MBL-HCV1 treatment significantly delayed time to viral rebound compared with placebo treatment ...


Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death, Dan Weng, Robyn Lynn Marty-Roix, Sandhya Ganesan, Megan K. Proulx, Gregory I. Vladimer, William J. Kaiser, Edward S. Mocarski, Kimberly Lea Pouliot, Francis Ka-Ming Chan, Michelle A. Kelliher, Phillip A. Harris, John Bertin, Peter J. Gough, Dmitry M. Shayakhmetov, Jon D. Goguen, Katherine A. Fitzgerald, Neal S. Silverman, Egil Lien 2014 University of Massachusetts Medical School

Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death, Dan Weng, Robyn Lynn Marty-Roix, Sandhya Ganesan, Megan K. Proulx, Gregory I. Vladimer, William J. Kaiser, Edward S. Mocarski, Kimberly Lea Pouliot, Francis Ka-Ming Chan, Michelle A. Kelliher, Phillip A. Harris, John Bertin, Peter J. Gough, Dmitry M. Shayakhmetov, Jon D. Goguen, Katherine A. Fitzgerald, Neal S. Silverman, Egil Lien

Katherine A. Fitzgerald

A number of pathogens cause host cell death upon infection, and Yersinia pestis, infamous for its role in large pandemics such as the "Black Death" in medieval Europe, induces considerable cytotoxicity. The rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effector Yersinia outer protein J (YopJ), is minimally affected by the absence of caspase-1, caspase-11, Fas ligand, and TNF. Caspase-8 is known to mediate apoptotic death in response to infection with several viruses and to regulate programmed necrosis (necroptosis), but its role in bacterially induced cell death is poorly understood. Here we provide genetic ...


Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death, Dan Weng, Robyn Lynn Marty-Roix, Sandhya Ganesan, Megan K. Proulx, Gregory I. Vladimer, William J. Kaiser, Edward S. Mocarski, Kimberly Lea Pouliot, Francis Ka-Ming Chan, Michelle A. Kelliher, Phillip A. Harris, John Bertin, Peter J. Gough, Dmitry M. Shayakhmetov, Jon D. Goguen, Katherine A. Fitzgerald, Neal S. Silverman, Egil Lien 2014 University of Massachusetts Medical School

Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death, Dan Weng, Robyn Lynn Marty-Roix, Sandhya Ganesan, Megan K. Proulx, Gregory I. Vladimer, William J. Kaiser, Edward S. Mocarski, Kimberly Lea Pouliot, Francis Ka-Ming Chan, Michelle A. Kelliher, Phillip A. Harris, John Bertin, Peter J. Gough, Dmitry M. Shayakhmetov, Jon D. Goguen, Katherine A. Fitzgerald, Neal S. Silverman, Egil Lien

Neal Silverman

A number of pathogens cause host cell death upon infection, and Yersinia pestis, infamous for its role in large pandemics such as the "Black Death" in medieval Europe, induces considerable cytotoxicity. The rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effector Yersinia outer protein J (YopJ), is minimally affected by the absence of caspase-1, caspase-11, Fas ligand, and TNF. Caspase-8 is known to mediate apoptotic death in response to infection with several viruses and to regulate programmed necrosis (necroptosis), but its role in bacterially induced cell death is poorly understood. Here we provide genetic ...


Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death, Dan Weng, Robyn Lynn Marty-Roix, Sandhya Ganesan, Megan K. Proulx, Gregory I. Vladimer, William J. Kaiser, Edward S. Mocarski, Kimberly Lea Pouliot, Francis Ka-Ming Chan, Michelle A. Kelliher, Phillip A. Harris, John Bertin, Peter J. Gough, Dmitry M. Shayakhmetov, Jon D. Goguen, Katherine A. Fitzgerald, Neal S. Silverman, Egil Lien 2014 University of Massachusetts Medical School

Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death, Dan Weng, Robyn Lynn Marty-Roix, Sandhya Ganesan, Megan K. Proulx, Gregory I. Vladimer, William J. Kaiser, Edward S. Mocarski, Kimberly Lea Pouliot, Francis Ka-Ming Chan, Michelle A. Kelliher, Phillip A. Harris, John Bertin, Peter J. Gough, Dmitry M. Shayakhmetov, Jon D. Goguen, Katherine A. Fitzgerald, Neal S. Silverman, Egil Lien

Robyn Marty-Roix

A number of pathogens cause host cell death upon infection, and Yersinia pestis, infamous for its role in large pandemics such as the "Black Death" in medieval Europe, induces considerable cytotoxicity. The rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effector Yersinia outer protein J (YopJ), is minimally affected by the absence of caspase-1, caspase-11, Fas ligand, and TNF. Caspase-8 is known to mediate apoptotic death in response to infection with several viruses and to regulate programmed necrosis (necroptosis), but its role in bacterially induced cell death is poorly understood. Here we provide genetic ...


A Multifactorial Role For P. Falciparum Malaria In Endemic Burkitt's Lymphoma Pathogenesis, Charles Torgbor, Peter Awuah, Kirk Deitsch, Parisa Kalantari, Karen A. Duca, David A Thorley-Lawson 2014 Tufts University School of Medicine

A Multifactorial Role For P. Falciparum Malaria In Endemic Burkitt's Lymphoma Pathogenesis, Charles Torgbor, Peter Awuah, Kirk Deitsch, Parisa Kalantari, Karen A. Duca, David A Thorley-Lawson

University of Massachusetts Medical School Faculty Publications

Endemic Burkitt's lymphoma (eBL) arises from the germinal center (GC). It is a common tumor of young children in tropical Africa and its occurrence is closely linked geographically with the incidence of P. falciparum malaria. This association was noted more than 50 years ago. Since then we have learned that eBL contains the oncogenic herpes virus Epstein-Barr virus (EBV) and a defining translocation that activates the c-myc oncogene. However the link to malaria has never been explained. Here we provide evidence for a mechanism arising in the GC to explain this association. Accumulated evidence suggests that eBL arises in ...


Epstein-Barr Virus (Ebv)-Lytic Cross-Reactive Influenza-A (Iav) Memory Cd8 T-Cells In Ebv Sero-Negative Middle-Aged Adults, Rabinarayan Mishra, Levi B. Watkin, Nuray Aslan, Anna Gil, Katherine Ruiz De Luzuriaga, Liisa K. Selin 2014 University of Massachusetts Medical School

Epstein-Barr Virus (Ebv)-Lytic Cross-Reactive Influenza-A (Iav) Memory Cd8 T-Cells In Ebv Sero-Negative Middle-Aged Adults, Rabinarayan Mishra, Levi B. Watkin, Nuray Aslan, Anna Gil, Katherine Ruiz De Luzuriaga, Liisa K. Selin

UMass Center for Clinical and Translational Science Research Retreat

EBV is a common human pathogen, which infects ~90% of people and establishes a life-long chronic infection. The clinical outcomes of acute infection can range from asymptomatic to severe immunopathology such as infectious mononucleosis (IM). However, for unknown reasons 5-10% of middle-aged adults (>35 years) remain EBV-seronegative (EBV-SN) when the virus infects the vast majority of people, and is actively shed at high titers during chronic infection. Here we show that EBV-SN (ASN) HLA-A2+ middle-aged adults possess a unique IAV-M1-GIL58-66 memory CD8 T-cell response that cross-reacts with EBV lytic epitopes that differs from teenage EBV-SN (TSN) (18-19 years) and EBV-seropositive ...


Acute Symptomatic Influenza A Virus (Iav) Infection In Humans Leads To Expansion Of Highly Diverse Cd8 T Cell Repertoires Crossreactive With Persistent Epstein Barr Virus (Ebv), Anna Gil, Rabinarayan Misha, Nuray Aslan, Liisa K. Selin 2014 University of Massachusetts Medical School

Acute Symptomatic Influenza A Virus (Iav) Infection In Humans Leads To Expansion Of Highly Diverse Cd8 T Cell Repertoires Crossreactive With Persistent Epstein Barr Virus (Ebv), Anna Gil, Rabinarayan Misha, Nuray Aslan, Liisa K. Selin

UMass Center for Clinical and Translational Science Research Retreat

The competence of T cell responses predominantly depends on how efficient T cell receptors (TCRs) are at recognizing antigenic epitopes. We show here that during acute severely symptomatic IAV infection there was an expansion of IAV-M1/EBV-BRLF1 and IAV-M1/EBV-BMLF1 double-tetramer+ cells directly ex-vivo in 5 HLA-A2+ patients. We questioned whether this expansion specific to these two different crossreactive responses would lead to alterations in the TCR repertoire of the IAV-M158 , EBV-BRLF1109 and -BMLF1280 from before, during and following acute IAV infection. Using staining with Vb MAb we found that T cell responses generated to these epitopes became surprisingly more ...


Severity Of Infectious Mononucleosis (Im) Correlates With The Frequency Of Crossreactive Influenza A Virus (Iav)-M1 And Epstein Barr Virus (Ebv)-Bmlf-1-Specific Cd8 T Cells, Nuray Aslan, Levi B. Watkin, Anna Gil, Katherine Luzuriaga, Liisa K. Selin 2014 University of Massachusetts Medical School

Severity Of Infectious Mononucleosis (Im) Correlates With The Frequency Of Crossreactive Influenza A Virus (Iav)-M1 And Epstein Barr Virus (Ebv)-Bmlf-1-Specific Cd8 T Cells, Nuray Aslan, Levi B. Watkin, Anna Gil, Katherine Luzuriaga, Liisa K. Selin

UMass Center for Clinical and Translational Science Research Retreat

During EBV-associated IM IAV-specific crossreactive memory T cells are activated and play a role in disease severity. In HLA-A2+ IM patients, influenza M158 (IAV-M1)-specific CD8 memory T cell responses crossreacted with two different EBV lytic epitopes, BMLF1280 (17/29) and BRLF1190 (19/20). Furthermore, 11/22 IM patients demonstrated some intra-viral crossreactivity between EBV-BRLF1 and -BMLF1 responses. Disease severity of IM directly correlated with significantly increased frequencies of crossreactive IAV-M1/EBV-BMLF1, IAV-M1, and EBV-BMLF1 specific CD8 cells, and with mean viral load over the first 5 weeks of infection. Disease severity did not correlate with BRLF1 or M1/BRLF1 ...


Crossreactive Epstein-Barr Virus (Ebv)-Influenza A Virus (Iav) Specific Cd8 Memory T Cells During Acute Symptomatic Iav Infection, Rabinarayan Mishra, Anna Gil, Nuray Aslan, Katherine Ruiz De Luzuriaga, Liisa K. Selin 2014 University of Massachusetts Medical School

Crossreactive Epstein-Barr Virus (Ebv)-Influenza A Virus (Iav) Specific Cd8 Memory T Cells During Acute Symptomatic Iav Infection, Rabinarayan Mishra, Anna Gil, Nuray Aslan, Katherine Ruiz De Luzuriaga, Liisa K. Selin

UMass Center for Clinical and Translational Science Research Retreat

We previously showed that crossreactivity is common between IAV and EBV in HLA-A2+ patients during infectious mononucleosis. IAV-M1-GIL58-66 specific CD8 T cells, along with expanded populations of IAV-M1-GIL58-66/EBV-BRLF-1109-117 -YVL and IAV-M1-GIL58-66/EBV-BMLF1280-288-GLC double-tetramer+ cells were detected directly ex-vivo in 5 HLA-A2+ patients. Altered IAV-M158-66, EBV-BRLF1119-117 and -BMLF1280-288 TCR repertoires were observed over the course of infection and in comparison to healthy donors. After culture, cells were sorted and analyzed by gene array in order to assess global changes in immune responses following different stimulations, either cognate or crossreactive, in different patient populations. M1-GIL and BRLF1-YVL specific cells had similar ...


Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death, Dan Weng, Robyn Lynn Marty-Roix, Sandhya Ganesan, Megan K. Proulx, Gregory I. Vladimer, William J. Kaiser, Edward S. Mocarski, Kimberly Lea Pouliot, Francis Ka-Ming Chan, Michelle A. Kelliher, Phillip A. Harris, John Bertin, Peter J. Gough, Dmitry M. Shayakhmetov, Jon D. Goguen, Katherine A. Fitzgerald, Neal S. Silverman, Egil Lien 2014 University of Massachusetts Medical School

Caspase-8 And Rip Kinases Regulate Bacteria-Induced Innate Immune Responses And Cell Death, Dan Weng, Robyn Lynn Marty-Roix, Sandhya Ganesan, Megan K. Proulx, Gregory I. Vladimer, William J. Kaiser, Edward S. Mocarski, Kimberly Lea Pouliot, Francis Ka-Ming Chan, Michelle A. Kelliher, Phillip A. Harris, John Bertin, Peter J. Gough, Dmitry M. Shayakhmetov, Jon D. Goguen, Katherine A. Fitzgerald, Neal S. Silverman, Egil Lien

GSBS Student Publications

A number of pathogens cause host cell death upon infection, and Yersinia pestis, infamous for its role in large pandemics such as the "Black Death" in medieval Europe, induces considerable cytotoxicity. The rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effector Yersinia outer protein J (YopJ), is minimally affected by the absence of caspase-1, caspase-11, Fas ligand, and TNF. Caspase-8 is known to mediate apoptotic death in response to infection with several viruses and to regulate programmed necrosis (necroptosis), but its role in bacterially induced cell death is poorly understood. Here we provide genetic ...


Phthalates And Phthalate Alternatives: Effects On Proliferative And Estrogenic Target Genes In Ishikawa Cells, Ranjani Sundar '15, Ping Yin, Serdar E. Bulun 2014 Illinois Mathematics and Science Academy

Phthalates And Phthalate Alternatives: Effects On Proliferative And Estrogenic Target Genes In Ishikawa Cells, Ranjani Sundar '15, Ping Yin, Serdar E. Bulun

Student Publications & Research

Phthalates are used as plasticizers in many of the products found in medical, household, and industrial applications. Much research has not been completed on the effects of these phthalates as potential endocrine disrupting chemicals (EDCs). As these chemicals are ingested, the mechanism by which they affect the reproductive system is largely unknown. The purpose of this study was to observe how 2 phthalates, Di-n-butyl phthalate (DBP) and Diisononyl phthalate (DINP), and 2 phthalate alternatives, Dioctyl terephthalate (DOTP) and BHT (butylated hydroxytoluene)affect uterine cells in comparison to a vehicle treatment and 17β-Estradiol treatment. Changes in expression of mRNA were observed ...


Alteration Of Intestinal Microbiota In Response To Induced Immune System, Hao Tran, Andrew T. Gewirtz, Benoit Chassaing 2014 Georgia State University

Alteration Of Intestinal Microbiota In Response To Induced Immune System, Hao Tran, Andrew T. Gewirtz, Benoit Chassaing

Georgia State Undergraduate Research Conference

No abstract provided.


Regulation Of Type Ii Responses In Lung Fibrosis And Systemic Autoimmunity: A Dissertation, Tia Bumpus Brodeur 2014 University of Massachusetts Medical School Worcester

Regulation Of Type Ii Responses In Lung Fibrosis And Systemic Autoimmunity: A Dissertation, Tia Bumpus Brodeur

GSBS Dissertations and Theses

Preclinical models of lupus indicate that T cell-B cell collaboration drives antinuclear antibody (ANA) production and sustains T cell activation. Autoreactive B lymphocytes are present in the normal repertoire but persist as ignorant or anergic cells. Mechanisms that normally limit T cell activation of autoreactive B cells remain incompletely resolved, but potentially include the absence of autoreactive effector T cell subsets and/or the presence of autoAgspecific regulatory T cells (Tregs). Several studies have addressed this issue by using experimental systems dependent on transgenic autoreactive B cells, but much less is known about the activation of autoreactive B cells present ...


Cd8+ T Cell And Nk Responses To A Novel Dengue Epitope: A Possible Role For Kir3dl1 In Dengue Pathogenesis: A Dissertation, Elizabeth Townsley 2014 University of Massachusetts Medical School

Cd8+ T Cell And Nk Responses To A Novel Dengue Epitope: A Possible Role For Kir3dl1 In Dengue Pathogenesis: A Dissertation, Elizabeth Townsley

GSBS Dissertations and Theses

Variation in the sequence of T cell epitopes between dengue virus (DENV) serotypes is believed to alter memory T cell responses during second heterologous infections contributing to pathology following DENV infection. We identified a highly conserved, novel, HLA-B57-restricted epitope on the DENV NS1 protein, NS126-34. We predicted higher frequencies of NS126-34-specific CD8+ T cells in PBMC from individuals undergoing secondary, rather than primary, DENV infection due to the expansion of memory CD8+T cells. We generated a tetramer against this epitope (B57-NS126-34TET) and used it to assess the frequencies and phenotype of antigen-specific T cells ...


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