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Search Results to Susan L Swain PhD

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Research and Professional Experience:

1976-1977 Lecturer, UCSD, La Jolla, CA
1976-1981 Assistant Research Biologist, UCSD
1981-1984 Associate Research Biologist, UCSD
1984-1989 Associate Professor of Biology in Residence, UCSD
1989-1995 Professor of Biology in Residence, UCSD
1985-1996 Member, UCSD Cancer Center, San Diego, CA
1996-2007 Director, Trudeau Institute, Saranac Lake, NY
1996-present Member, Trudeau Institute, Saranac Lake, NY
1996-2007 Edward C. Brewster Chair, Trudeau Inst., Saranac Lake, NY
1998-present Adjunct Professor, Dept of Micro, Immunol & Mol. Gen, Albany Medical College, Albany, NY
2001-present Adjunct Professor, University of Vermont College of Medicine, Burlington, VT
2003-2007 President,Trudeau Institute, Saranac Lake, NY
2008-2010 President Emeritus, Trudeau Institute
2010 Professor of Pathology, UMASS Medical School, Worcester, MA

Study Sections and Advisory Panels: Past:NIH Immunobiology Study Section (1984-1988); AIDS Basic Research Advisory Committee, NIAID (1990-1992); National Taskforce on Aging, NIA/NIAID (1994); FY1997 AIDS Planning Committee (1995); Ad Hoc Member, Board of Scientific Councilors NIAID (1995, 2000); Scientific Advisory Board, Inst. for Advanced Studies in Immunol. Aging (1996-1999); Reviewer's Reserve, NIH (1988-present); NHLBI SCOR Review in Asthma Panel (2001); Board of Scientific Councilors, National Institute of Aging (2001-2006), Arthritis Review Panel in Cellular Immunology (1996-1998); Board of Trustees, Ordway Institute, Albany, NY (2001-2005), External Advisory Committee, University of Montana COBRE (2005-2007). External Advisory Board Duke University Dept. of Immunology (2008), Current: Board of Directors La Jolla Institute of Allergy and Immunology (2004-present), Selection Committee Albany Medical Prize (2005-present), External Advisory Committee (EAC): Wistar BAA (2006-present) and Dartmouth University COBRE (2007-present). National Advisory Council on Aging 2008-2012, Scientific Advisory Board La Jolla Institute of Allergy and Immunology 2008-present, Advisory Group Aeras 2007-present, Distinguished Editorial Panel NIAID (2009), Council, NIAID (Ad Hoc, 2009)

Editorial Boards:Past: Lymphokines (1985-1988); Journal of Immunology Associate Editor (1985-1987), Section Editor (1987-1991), Primary Reviewer (1997-present); International Immunology (1988-present); Cellular Immunology (1988-present); Cell (1990-1992); Current Opinion in Immunology, issue editor (1994, 1996, 2003, 2009); Current Biology (1994), Journal of Experimental Medicine (1997-2008), Current: Deputy Editor, Journal of Immunology 2008-2012, Faculty of 1000, Section Leader (2002-present).

Meeting Organization: Workshop on T and B Cell Memory (1993, 1998); Midwinter Immunology Conference Council (1992), Midwinter Conference of Immunologists (1996); Keystone Symposium on Lymphocyte Activation (1996); International Cytokine Conference (1997); Delegate IUIS (2002-2006), Workshop on Immunity and Aging, Trudeau Institute, NY (2004); Cold Spring Harbor Vaccine Meeting (2005, 2007, 2009), Keystone Symposium on Immunological Memory (2007), FASEB Summer Conference (2008, 2010).

Community Service:American Association of Immunology: Committee on Women (1988-1994), Program Committee (1988-1994); Chair, T Cell Block for FASEB Meeting (1992-1995); Nominations Committee (Elected, 1991, 1995,1996). Publication Committee (Elected, 1994-1998).

Elected Positions: Council Member, American Association of Immunologists (1999-2006); Electorate Nominating Committee of the Section on Medical Sciences, AAAS (2004); President, American Association of Immunologists (2004).

Honors and Awards:Phi Beta Kappa, Magna Cum Laude, B.A. (1968); Sigma Xi (1972); Established Investigator, American Heart Association (1981-1986); NIH Merit Award (1995, 2005); New York State Woman of Distinction (2002); Fellow of the American Association for Advancement of Science (2007); American Association of Immunologists Lifetime Achievement Award (2010).

Dr. Susan SwainOur past research has focused on defining the cellular and molecular mechanisms by which CD4 T cells contribute to immunity. In particular we have 1) Defined, generated and determined the function of T cell subsets at the effector stage; 2) Studied the requirements for the generation of long-live memory CD4 T cells and their role in protection against influenza infection and 3) Analyzed the defects that develop in T cell function with aging and the causes of those defects.

Our top priorities at this time are to discover new basic cellular and molecular mechanisms that are used by memory CD4 T cells to provide effective immunity to infectious diseases and to better define the age-associated defects in CD4 T cells that contribute to poor immunity of the aged and to discover strategies to overcome those defects.

Post Docs

An entry level postdoctoral position is open immediately in the laboratory of Dr. Susan L. Swain to study the factors that control the development and survival of CD4 and CD8 T cell memory. Graduate student experience with tissue culture, in vitro assay, flow cytometry, experience in mouse models on infectious disease and a knowledge of cellular and molecular immunology are all strongly desired.

Rotation Projects

Rotations: Projects in the following areas

CD4 T cell memory. We can generate in vitro CD4 T cells that are for all extents and purposes identical to the memory CD4 T cells observed in vivo. In situ memory CD4 T cells persist at very low frequency and in most instances it is difficult to analyze them thoroughly using tetramer or multimer reagents both because of their low frequency and the relatively low specific affinity of the Class II reagents for the TcR. Being able to generate “recent” memory cells in vitro gives us the opportunity to analyze in detail the mechanisms by which memory CD4 T cells may contribute to secondary immunity and immune protection. Once identified. will determine if particular pathways are relevant in situ. We have discovered that memory CD4 T cells are superior in protection to those from the primary response and that they display pleitropic functions that have not been previously identified.

Cytotoxic CD4 Effectors. One unexpected function of CD4 T cells we identified is robust, perforin-dependent cytotoxic activity (7, 16). Cytotoxic activity by CD4 T cells has been reported in response to several infections, but its significance has not heretofore been established. We find that “Th1 polarized” CD4 effectors and more relevantly the CD4 effectors found in the lung following influenza infection, are able to kill infected or peptide-pulsed Class II-bearing targets and we find that this perforin dependent activity can work together with antibody to provide protection against lethal influenza challenge in otherwise unprimed mice (17). We also will determine when memory CD4 T cells re-express cytotoxic activity following in vivo challenge and how cytotoxic killing contributes to the memory cell mediated protection. We want to analyze how the program of cytotoxicity is induced in these “ThCTL”.

Memory CD4 Cells Enhance an Innate Response. Memory cells can act by becoming secondary effectors but they are best characterized by their ability respond rapidly even to low antigen doses, by producing cytokines and chemokines and it is assumed that these initial abilities are key to memory cell activity. However this assumption has not been directly demonstrated and the mechanisms involved and how they might contribute to immunity have not been elucidated. We find that restimulation of memory CD4 T cells leads to a markedly enhanced early innate response to influenza infection both in the lung and systemically (17). This response peaks 2-3 days after infection and is transient. We see enhanced production of IL-6 locally and systemically and enhanced production a broad spectrum of innate inflammatory mediators in the lung. We hope to determine in detail the pathways leading to optimum memory T cell-induced innate responses. We suggest a concurrent activation of CD4 memory cells may be an effective adjuvant for vaccination and will be testing this hypothesis as well as mechanisms that lead to viral control over the next couple of years.

Aging and Immunity: The study of the impact of aging on CD4 T cell function at the naïve and memory stages has lead us to better understanding of fundamental aspects of T cell behavior in addition to providing important information about what vaccine approaches are most likely to be successful for the aged.

Nature of CD4 Aging “Defects”. We have identified multiple levels at which aged naïve CD4 T cells are defective including initial early response to TcR triggering, IL-2 production, expansion and effector generation. The defects in helper function and in the 20 response of memory cells generated from aged naïve CD4 T cells are particularly dramatic. In recent studies we have recapitulated memory age-associated defects in recently generated memory cells in vitro (23). In vitro aged memory cells are markedly defective in production of particular cytokines, IL-4, IL-5 and IL-2, while others are little affected (IFNg, IL-10, TNF), suggesting the aging “defect” may be restricted to loss of potential to make certain CD4 T cell subsets, such as those responsible for help to B cells .We will pursue this hypothesis both in vitro and in vivo.

We have found that aged naïve CD4 T cells are in fact longer-lived than their naïve counterparts (23). We find that reduced expression of Bim, a proapoptotic protein, is responsible for this increase in lifespan and that the increase in lifespan is required for the development of aging defects. We are now investigating the factors that regulate Bim expression.

Enhancement by Inflammatory Cytokines. We have shown that the defective effector generation responses of naïve CD4 T cells from aged animals can be overcome by IL-2 and by proinflammatory cytokines, in particular a mix of IL-1, IL-6 and TNF (20,21). We want to determine the extent to which the inflammatory cytokines can reverse the heritable aging defects and restore functional memory generation. We have developed in vitro models to test the generation of effectors and memory. In these models we are evaluating TLR agonists for their ability to restore aged naïve CD4 responses to peptide-pulsed derived dendritic cells (DC). Pre-incubation of DC with many TLR agonists, enhances expansion of the responding aged naïve CD4 T cells via a mechanism dependent on IL-6 that acts in part by increasing survival of the developing effector population. We plan to use this model to identify the extent of the rescue and what pathways and mechanisms contribute with the ultimate goal of evaluating whether specific TLR stimulation or stimulation of specific pathways might improve the response of the elderly to vaccines. We want to see if we can reproduce this model with human naïve CD4 T cells and DC derived from peripheral blood and if TLR agonists can also enhance those responses.

One or more keywords matched the following items that are connected to Swain, Susan

Item TypeName
Academic Article From naive to memory T cells.
Academic Article Antigen-independent changes in naive CD4 T cells with aging.
Academic Article Age-related changes in CD4 T cells of T cell receptor transgenic mice.
Academic Article From naive to effector--alterations with aging.
Academic Article T cell memory.
Academic Article From naive to memory. Development and regulation of CD4+ T cell responses.
Academic Article Long-term CD4+ memory T cells from the spleen lack MEL-14, the lymph node homing receptor.
Academic Article Transforming growth factor-beta enhances the in vivo effector function and memory phenotype of antigen-specific T helper cells in experimental autoimmune encephalomyelitis.
Academic Article Helper T cell memory: more questions than answers.
Academic Article The generation and maintenance of memory T and B cells.
Academic Article Qualitative changes accompany memory T cell generation: faster, more effective responses at lower doses of antigen.
Academic Article The defects in effector generation associated with aging can be reversed by addition of IL-2 but not other related gamma(c)-receptor binding cytokines.
Academic Article CD4 T-cell memory can persist in the absence of class II.
Academic Article Two distinct stages in the transition from naive CD4 T cells to effectors, early antigen-dependent and late cytokine-driven expansion and differentiation.
Academic Article CD4(+) T cell effectors can become memory cells with high efficiency and without further division.
Academic Article Regulation of T cell subsets from naive to memory.
Academic Article Regulation of memory CD4 T cells: generation, localization and persistence.
Academic Article Regulation of the generation and maintenance of T-cell memory: a direct, default pathway from effectors to memory cells.
Academic Article CD4 T cell memory derived from young naive cells functions well into old age, but memory generated from aged naive cells functions poorly.
Academic Article Helper T cell differentiation.
Academic Article T cell responses to influenza virus infection: effector and memory cells.
Academic Article Class II-independent generation of CD4 memory T cells from effectors.
Academic Article IL-7: maintaining T-cell memory and achieving homeostasis.
Academic Article Repeated stimulation of CD4 effector T cells can limit their protective function.
Academic Article Thanks for the memory!
Academic Article CD4+ T-cell memory: generation and multi-faceted roles for CD4+ T cells in protective immunity to influenza.
Academic Article Critical role of cognate interactions in the response of small, high-density B cells.
Academic Article Unique ability of activated CD4+ T cells but not rested effectors to migrate to non-lymphoid sites in the absence of inflammation.
Academic Article Accumulation of NFAT mediates IL-2 expression in memory, but not naïve, CD4+ T cells.
Academic Article Influencing the fates of CD4 T cells on the path to memory: lessons from influenza.
Academic Article Bone marrow precursor cells from aged mice generate CD4 T cells that function well in primary and memory responses.
Academic Article Functionally diverse subsets in CD4 T cell responses against influenza.
Academic Article T-cell immunosenescence: lessons learned from mouse models of aging.
Academic Article The potential of CD4 T-cell memory.
Academic Article Antigen presentation and the regulation of CD4 memory generation to influenza.
Academic Article Characterization of antigen-specific CD4+ effector T cells in vivo: immunization results in a transient population of MEL-14-, CD45RB- helper cells that secretes interleukin 2 (IL-2), IL-3, IL-4, and interferon gamma.
Academic Article Hallmarks of CD4 T cell immunity against influenza.
Academic Article Effect of age on naive CD4 responses: impact on effector generation and memory development.
Academic Article Control of innate immunity by memory CD4 T cells.
Academic Article Memory CD4+ T cells protect against influenza through multiple synergizing mechanisms.
Academic Article Memory CD4+ T-cell-mediated protection depends on secondary effectors that are distinct from and superior to primary effectors.
Academic Article Germinal center B cells in Peyer's patches of aged mice exhibit a normal activation phenotype and highly mutated IgM genes.
Academic Article Regulation of the development of helper T cell subsets.
Academic Article IL-7 promotes the transition of CD4 effectors to persistent memory cells.
Academic Article Generation and in vivo persistence of polarized Th1 and Th2 memory cells.
Academic Article Naive versus memory CD4 T cell response to antigen. Memory cells are less dependent on accessory cell costimulation and can respond to many antigen-presenting cell types including resting B cells.
Academic Article Both naive and memory CD4 T cell subsets become anergic during MAIDS and each subset can sustain disease.
Academic Article Memory effectors: a potent, IL-4-secreting helper T cell population that develops in vivo after restimulation with antigen.
Academic Article T-cell memory: new perspectives.
Academic Article CD4 T cell responses to influenza infection.
Academic Article CD4+ T cell subsets. Lymphokine secretion of memory cells and of effector cells that develop from precursors in vitro.
Academic Article Unexpected prolonged presentation of influenza antigens promotes CD4 T cell memory generation.
Academic Article The significance of T-B collaboration across haplotype barriers.
Academic Article Rapid default transition of CD4 T cell effectors to functional memory cells.
Academic Article The effector to memory transition of CD4 T cells.
Academic Article Memory CD4+ T cells induce innate responses independently of pathogen.
Academic Article Expanding roles for CD4? T cells in immunity to viruses.
Academic Article Grand challenges in immunological memory.
Academic Article Memory CD4 T cell-mediated immunity against influenza A virus: more than a little helpful.
Academic Article Multipronged CD4(+) T-cell effector and memory responses cooperate to provide potent immunity against respiratory virus.
Academic Article The cytokines IL-4, IFN-gamma, and IL-12 regulate the development of subsets of memory effector helper T cells in vitro.
Academic Article CD4 T cell development and cytokine polarization: an overview.
Concept Immunologic Memory
Academic Article Effector CD4 T-cell transition to memory requires late cognate interactions that induce autocrine IL-2.
Academic Article New Insights into the Generation of CD4 Memory May Shape Future Vaccine Strategies for Influenza.
Academic Article Short-Lived Antigen Recognition but Not Viral Infection at a Defined Checkpoint Programs Effector CD4 T Cells To Become Protective Memory.
Academic Article IL-15 supports the generation of protective lung-resident memory CD4 T cells.
Academic Article Pathogen Recognition by CD4 Effectors Drives Key Effector and Most Memory Cell Generation Against Respiratory Virus.
Academic Article Memory CD4 T cell-derived IL-2 synergizes with viral infection to exacerbate lung inflammation.
Academic Article CD25-Targeted IL-2 Signals Promote Improved Outcomes of Influenza Infection and Boost Memory CD4 T Cell Formation.
Academic Article Influenza Vaccine-Induced CD4 Effectors Require Antigen Recognition at an Effector Checkpoint to Generate CD4 Lung Memory and Antibody Production.

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