2009년 대한면역학회 추계학술대회에 귀하를 초대합니다 .

2009년 추계 학술대회가 11월 9, 10일 양일간 서울교육문화회관에서 열립니다.
Dr. Richard A. Flavell, Dr. Jeffrey A. Bluestone을 비롯한 국내외 저명한 면역학자들을 초청하여 국제적인 학술 대회를 개최함으로써 우리나라 면역학 연구의 위상을 증진시키고 그 중요성을 대내외적으로 널리 알리고자 합니다.

내실있고 성공적인 대한면역학회 추계학술대회가 될 수 있도록 많은 관심과 참여 부탁 드립니다.

※ 사전등록 마감일이 11월 3일(화)로 연장되었습니다.

Dr. Richard A. Flavell is one of the greatest figures in the field of immunology and life science in general. He earned a B.Sc. and a Ph.D. in Biochemistry from the University of Hull, Great Britain, and was a postdoctoral fellow at EMBO. After serving on the faculty of the University of Amsterdam and the National Institute for Medical Research in London, he joined Biogen. Since 1988, Dr. Flavell has served as a chair of the Section of Immunobiology at the Yale School of Medicine and as an investigator at the Howard Hughes Medical Institute. His appointment to a Sterling Professorship is one of the highest tributes Yale gives to faculty members. Areas of research include but are not restricted to the followings: CD4 T cell differentiation, autoimmunity and immune regulation, innate immunity, and apoptosis. Representative accomplishments are (1) interaction of CD40-CD40L in the activation of T and B cells (2) roles and mechanisms of signaling molecules and transcription factors such as GATA-3, JunB, MAPK, JNK, and Notch in Th1/Th2 differentiation (3) roles of TGF, TGF receptors, TNF, TRANCE, IL-2, and regulatory T cells in the autoimmunity and immune regulation, in particular in the pathogenesis of autoimmune diseases such as autoimmune diabetes, rheumatoid arthritis, and EAE (4) roles of TLR3, TLR5, IRAK, RICK, NOD and inflammasome (5) roles of apoptosis and caspases in the immune responses. Dr. Flavell published more than 700 papers, many of which are published in the prestigious journals such as Cell, Science and Nature.

Recent publications

1. Crucial role for the Nalp3 inflammasome in the immunostimulatory properties of aluminum adjuvant. Nature 2008, 453(7198):1122-1126.
2. Regulatory T-cell functions are subverted and converted owing to attenuated Foxp3 expression. Nature 2007, 445(7129):766-770.
3. Caspases 3 and 7: key mediators of mitochondrial events of apoptosis. Science 2006, 311(5762):847-851.
4. Interchromosomal associations between alternatively expressed loci. Nature 2005 435(7042):637-645.
5. Nod2-dependent regulation of innate and adaptive immunity in the intestinal tract. Science 2005, 307(5710):731-734.

Prof. Jeffrey Bluestone is the founding director of the Immune Tolerance Network (ITN) since 1999 and the director of the Diabetes Center at UCSF, where he holds the A. W. and Mary Margaret Clausen Distinguished Professorship in Diabetes and Endocrinology. Prof. Bluestone is an immunologist highly recognized for his significant contributions toward understanding of the biological basis for immunologic tolerance, and helped elucidate regulation of T cell activation. He has pioneered the development of hOKT3-gamma (Ala-Ala), a humanized form of the anti-CD3 monoclonal antibody that is now in clinical trials for early diabetes, psoriatic arthritis and islet transplantation. His recent research has centered on understanding and altering the positive or negative signals delivered by the antigen-specific T cell receptor and co-stimulatory signals such as CTLA-4, PD-1 and Notch, which was published in Nature, Nature Medicine, Nature Immunology, Immunity, and other internationally renowned journals. Studies from his laboratory have also identified the critical role for CD4+CD25+ Treg cells in the regulation of autoimmune diabetes. Using the insights gained from the basic processes that control T cell activation and tolerance, Dr. Bluestone hopes to develop a new generation of tolerogenic drugs that will turn off selected parts of the immune system, leaving the disease-fighting capabilities intact.

Recent publications

1. Instability of the transcription factor Foxp3 leads to the generation of pathogenic memory T cells in vivo. Nat. Immunol. 2009, 10(9):1000-1007.
2. Central role of a defective IL-2 production in triggering islet autoimmune destruction. Immunity 28:687-97, 2008.
3. A novel myelin P0-specific T cell receptor transgenic mouse develops a fulminant autoimmune peripheral neuropathy. J. Exp. Med. 2009, 206(3):507-514.
4. Tang, Q., Adams , J.Y., Tooley, A.J., Bi, M., Fife , B.T., Serra, P., Santamaria, P., Locksley, R.M., Krummel, M.F., Bluestone, J.A. Visualizing regulatory T cell control of autoimmune responses in nonobese diabetic mice. Nat. Immunol. 7:83-92, 2006.
5. Tyrosine kinase inhibitors reverse type 1 diabetes in nonobese diabetic mice. Proc. Natl. Acad. Sci. U.S.A. 2008, 105(48):18895-18900.

Special Lecture I

* Peter J. Lane

Dr. Peter Lane has received an MBChB degree at Edinburgh University Medical School, UK in 1980 and a Ph.D. degree at University of Birmingham, UK in 1987. Dr. Lane has served as a Member at Basel Institute for Immunology, Switzerland between 1990 ~ 1996, and is currently Professor of Immunology, Department of Immunity and Infection, University of Birmingham, UK. Dr. Lane is interested in the cellular and molecular signals that control the organization of lymphoid tissue microenvironments where T cells are sustained (memory) and provide help to B cells and other cells. His research initially focused on the signals and cells that regulate T cell help or memory for antibody production (CD28 and CD40), and maintain CD4 T cell memory (CD30 and OX40). He has investigated in detail the function of accessory cells that express CD4 as well as chemokine receptor CXCR4.

Recent publication

1. Generating intrathymic microenvironments to establish T-cell tolerance. Nat. Rev. Immunol. 2007, 7:954-963.
2. Function of CD4+CD3- cells in relation to B- and T-zone stroma in spleen. Blood 2007, 109:1602-1610.
3. RANK signals from CD4(+)3(-) inducer cells regulate development of Aire-expressing epithelial cells in the thymic medulla. J. Exp. Med. 2007, 204:1267-1272.

Special Lecture II

* Yang-Xin Fu

Dr. Yang-Xin Fu has been studying a cross-talk between immune cells and stromal cells which establish a microenvironment that is necessary for lymphoid tissue development, central and peripheral tolerance, and efficient migration of immune responses. To uncover molecular mechanisms underlying the interactions between lymphocytes and stromal cells, Dr. Fu proposed that lymphotoxin (LT) from T cells and LTR on stromal cells establish a lymphoid microenvironment. More specifically, a set of distinct adhesion molecules and tissue chemokines from stromal cells are regulated by lymphocytes for a flexible, delicate, and rapid immune response inside and outside lymphoid tissues. His study has revealed that lymphotoxin (LT), TNF, and LIGHT (another ligand for LT receptor) are key cytokines for establishing organized lymphoid structures inside and outside lymphoid organs/tissues that are critical for lymphocytes development and various immune responses.

Recent publication

1. Adaptive immune cells temper initial innate responses. Nat. Med. 2007, 13:1248-1252.
2. B and T lymphocyte attenuator regulates CD8+ T cell-intrinsic homeostasis and memory cell generation. Nat. Immunol. 2007, 8:162-171.
3. Recruitment and activation of naive T cells in the islets by lymphotoxin beta receptor dependent tertiary lymphoid structure. Immunity 2006, 25:399-409.

Special Lecture III

* Michael G. McHeyzer –Williams

Dr. Michael McHeyzer-Williams received a Ph.D. in Immunology in 1991 from the Walter and Eliza Hall Institute of Medicine, University of Melbourne, Australia. As a Lucille P. Markey Fellow, Dr. McHeyzer-Williams undertook post-doctoral work in the Immunology Department at Stanford University Medical Center in 1992. In 1995, he was appointed as Assistant Professor in Immunology at Duke University Medical Center in Durham, NC. Since 2001, Dr. McHeyzer-Williams has continued his work at The Scripps Research Institute in La Jolla, CA, and now is Professor in Immunology. His research focuses on regulating adaptive immunity, seeking to define the cellular and molecular details of the major development and checkpoints that regulate helper T and antigen-specific B cell fate decisions in vivo. He has recently extended his studies to the earliest innate immune events that initiate and shape the adaptive immune response to understand the rules that control adaptive immunity and better design safe and effective protein subunit vaccines.

Recent publication

1. Follicular helper T cells: lineage and location. Immunity 2009, 30(3):324-335.
2. The function of follicular helper T cells is regulated by the strength of T cell antigen receptor binding. Nat. Immunol. 2009, 10(4):375-384.
3. Vaccine adjuvants alter TCR-based selection thresholds. Immunity 2008, 28(5):698-709.

Special Lecture IV

* Jae Ung Jung

Dr. Jae Ung Jung received his Ph.D. at the UC Davis in 1989. After a postdoctoral training at the New England Primate Research Center, Harvard Medical School, he was promoted as an associate professor and tenured as a full professor at the Department of Microbiology and Genetics, Harvard Medical School. Since 2008, Dr. Jung has served as a professor and chairman of the Department of Molecular Microbiology and Immunology, USC Keck Medical School. His research focuses on understanding the molecular mechanisms of lymphoproliferative diseases by the gamma-2 herpesviruses and developing animal models for human diseases. His research has helped to understand viral immune evasion strategies and mechanisms of innate immune responses against virus. Currently, he extends his research to the area of molecular mechanisms of viral infection-related autophagy. His research group identified UVRAG that plays an important role in the initiation of autophagy and the development of cancer.

Recent publication

1. Beclin1-binding UVRAG targets the class C Vps complex to coordinate autophagosome maturation and endocytic trafficking. Nat. Cell Biol. 2008, 10(7):776-787.
2. TRIM25 RING-finger E3 ubiquitin ligase is essential for RIG-I-mediated antiviral activity. Nature 2007, 446:916-920.
3. Autophagic and tumor suppressor activity of a novel Beclin1-binding UVRAG. Nat. Cell Biol. 2006, 8:688-698.

Special Lecture V

* Paola Ricciardi-Castagnoli

Since she received her Ph.D. in immunology from the University of Louvain (Belgium) in 1974, Dr. Ricardi-Castagnoli has been a world-renowned immunologist. Her research has been mostly focused on the area of dendritic cell immunology and scientific contribution has been recognized by journal citations. She is recognized as one of the most cited immunologists during the last 10 years with 5,172 citations for 58 papers with an average of 89 citations (http://www.in-cites.com/nobel/2006-imm-top100.html) in-cites ESI (essential science indicators) source for 1996-2006. Dr. Ricardi-Castagnoli is currently working as a Scientific Director of Singapore Immunology Network SIgN (BMSI) A-STAR at Biopolis, Singapore and serves as a vice-president of the Singapore Society of Immunology (SII).

Recent publication

1. TPL-2 negatively regulates interferon-beta production in macrophages and myeloid dendritic cells. J. Exp. Med. 2009, 206(9):1863-1871.
2. CD14 regulates the dendritic cell life cycle after LPS exposure through NFAT activation. Nature 2009, 460(7252):264-268.
3. How do human cells react to the absence of mitochondrial DNA? PloS One 2009, 4(5): e5713.

Special Lecture VI

* Polly Matzinger

As one of the most famous figures in immunology, Dr. Polly Matzinger has been focusing on the following 3 fundamental topics related to the T cell tolerance and memory: 1) What turns an immune response on and off? 2) How does the immune system remember its past encounters? 3) What regulates the effector class of an immune response? Her laboratory is currently working on the basis of a new theoretical view of the immune system. The new model starts with the idea that the driving force for an immune response is not the recognition of foreign antigen but the recognition of “danger”. The idea is that incoming viruses, bacteria, worms, and other pathogens create damage in the tissues they inhabit. These tissues relay alarm signals to activate the local sentries (the dendritic cells) to initiate immune responses. Dr. Matzinger’s group is trying to find the tissue-generated alarm signals and also studying several implications of the model in such areas as pregnancy, autoimmune disease, and transplantation.

Recent publication

1. Interleukin 7 signaling in dendritic cells regulates the homeostatic proliferation and niche size of CD4+ T cells. Nat. Immunol. 2009, 10(2):149-157.
2. Antigen-specific T-T interactions regulate CD4 T-cell expansion. Blood 2008, 112(4):1249-1258.
3. CD4 cells can be more efficient at tumor rejection than CD8 cells. Blood 2007, 109(12):5346-5354.