Bulletin of the American Physical Society
2009 APS March Meeting
Volume 54, Number 1
Monday–Friday, March 16–20, 2009; Pittsburgh, Pennsylvania
Session Q7: Physics of the Immune System |
Hide Abstracts |
Sponsoring Units: DBP Chair: Aaron Dinner, University of Chicago Room: 407 |
Wednesday, March 18, 2009 11:15AM - 11:51AM |
Q7.00001: How T lymphocytes see antigen Invited Speaker: Complex organisms, like humans, have an adaptive immune system that enables us to do battle with diverse pathogens. This flexible system can also go awry, and many diseases are the direct consequence of the adaptive immune system failing to discriminate between markers of self and non-self. The orchestrators of adaptive immunity are a class of cells called T lymphocytes (T cells). T cells recognize minute numbers of molecular signatures of pathogens, and T cell recognition of these molecular markers of non-self is both specific and degenerate. The specific (yet, cross-reactive), diverse, and self-tolerant T cell repertoire is designed in the thymus. I will describe how an approach that brings together theoretical and computational studies (rooted in statistical physics) with experiments (carried out by key collaborators) has allowed us to shed light on the mechanistic principles underlying how T cells respond to pathogens in a digital fashion (``on'' or ``off''), and how this molecular machinery coupled with frustration (a la spin glasses) plays a key role in designing the special properties of the T cell repertoire during development in the thymus. [Preview Abstract] |
Wednesday, March 18, 2009 11:51AM - 12:27PM |
Q7.00002: Physical Theory of Vaccine Design for Influenza and Dengue Fever Invited Speaker: The immune system normally protects the human host against death by infection. I will introduce a physical theory of the evolutionary dynamics that occurs in the antibody-mediated and T cell-mediated immune responses. The theory will be used to provide a mechanism for original antigenic sin, wherein an initial exposure to antigen can degrade the response of the immune system upon subsequent exposure to related, but different, antigens. A new order parameter to characterize antigenic distance will be introduced from the theory. This order parameter predicts effectiveness of the influenza vaccine more reliably than do results from animal model studies currently used by world health authorities. I will discuss how this order parameter might be a valuable new tool for making vaccine-related public health policy decisions. Next, I will briefly discuss dengue fever. Infection with, or vaccination against, one of the four serotypes of dengue fever typically increases susceptibility to dengue hemorrhagic fever from one of the other three serotypes. I will present a physical theory of this immunodominance and use this theory to quantify the predicted mitigation of immunodominance in a novel formulation of the dengue vaccine. [Preview Abstract] |
Wednesday, March 18, 2009 12:27PM - 1:03PM |
Q7.00003: Fast, continuous recirculation of germinal center B cell populations enhances robustness of immune response towards varying pathogens Invited Speaker: Germinal centers (GCs) are dynamic microstructures that form in lymphatic tissues during immune responses. There, B cells undergo rapid proliferation and mutation of their B cell receptors (BCRs). Selection of B cells bearing BCRs that bind to the pathogen causing the immune response ultimately leads to BCRs that, when secreted as antibodies, form a new, effective, and pathogen specific antibody repertoire. However, the details of this evolutionary process are poorly understood, since currently available experimental techniques do not allow for direct observation of the prevailing mechanisms [Or-Guil et al., Imm.Rev. 2007]. Based on optimality considerations, we put forward the assumption that GCs are not isolated entities where evolutionary processes occur independently, but interconnected structures which allow for continuous exchange of B cells. We show that this architecture leads to a system whose response is much more robust towards different antigen variants than a set of independently working GCs could ever be. We test this hypothesis by generating our own experimental data (time course of 3-D volume distribution of GCs, analysis of high-throughput BCR sequences), and show that available data is consistent with the outlined hypothesis. [Preview Abstract] |
Wednesday, March 18, 2009 1:03PM - 1:39PM |
Q7.00004: Fish Immunology Invited Speaker: |
Wednesday, March 18, 2009 1:39PM - 2:15PM |
Q7.00005: Genetic Circuit Architectures Underlying Cell Fate Choices for Immunity Invited Speaker: Antigen stimulated B cells follow an unusual developmental trajectory that transiently passes through a germinal center state, which promotes receptor affinity maturation and immunoglobulin class switching, before terminally differentiating into antibody secreting plasma cells. It was found that graded expression of the transcription factor IRF-4 regulates cell fate, but the relationship between antigen receptor signaling, the network of interactions with IRF-4, and cell fate was not known. This talk describes models that link ligand-receptor avidity with cell fate. The models have been validated experimentally by directly varying the levels and kinetics of IRF-4 accumulation. Furthermore, signaling through the antigen receptor is demonstrated to control the expression of IRF-4 and in turn the frequency of B cells that undergo class switching before differentiating into plasma cells. These findings provide an explanation for experiments that measure B cell numbers in transgenic mice. The architecture of our regulatory circuit provides a general mechanism for quantitative variations in a signal to be translated into a binary cell-fate choice involving transient expression of one of the two developmental fates. In collaboration with Aryeh Warmflash, Ying Li, Roger Sciammas, and Harinder Singh, The University of Chicago. [Preview Abstract] |
Follow Us |
Engage
Become an APS Member |
My APS
Renew Membership |
Information for |
About APSThe American Physical Society (APS) is a non-profit membership organization working to advance the knowledge of physics. |
© 2024 American Physical Society
| All rights reserved | Terms of Use
| Contact Us
Headquarters
1 Physics Ellipse, College Park, MD 20740-3844
(301) 209-3200
Editorial Office
100 Motor Pkwy, Suite 110, Hauppauge, NY 11788
(631) 591-4000
Office of Public Affairs
529 14th St NW, Suite 1050, Washington, D.C. 20045-2001
(202) 662-8700