Abstract

HUMAN IMMUNE CELL MATURATION DURING ONTOGENY AND INFECTION This program represents a new and promising collaboration between five investigators at the University of California, San Francisco and Stanford University, all of whom work on complementary aspects on human immunology. The five problems addressed in the individual units investigate regulatory mechanisms influencing human immune cell maturation during ontogeny and infection. Each sit describes a collaboration with at least one other investigator in the program and reflects the shared interests and expertise of the investigators involved. All of our laboratories are committed to studying the human immune response. This commitment arises broth from an interest in human disease and the fact that several of use study systems that are markedly different in humans than in the prevailing mouse model systems. Together the proposed projects define unique aspects of the human immune response in comparison to murine and non-human primate systems, analyze the role of signaling and membrane traffic in regulation of human lymphoid development and study the effects of infectious diseases in humans on lymphoid maturation and function.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
5P01AI045865-03
Application #
6374233
Study Section
Special Emphasis Panel (ZAI1-SCO-I (M1))
Program Officer
Nabavi, Nasrin N
Project Start
1999-09-30
Project End
2003-08-31
Budget Start
2001-09-01
Budget End
2002-08-31
Support Year
3
Fiscal Year
2001
Total Cost
$803,985
Indirect Cost

  Institution

Name
University of California San Francisco
Department
Miscellaneous
Type
Schools of Medicine
DUNS #
073133571
City
San Francisco
State
CA
Country
United States
Zip Code
94143

  Publications

Chen, Liguang; Apgar, John; Huynh, Lang et al. (2005) ZAP-70 directly enhances IgM signaling in chronic lymphocytic leukemia. Blood 105:2036-41
Crotzer, Victoria L; Mabardy, Allan S; Weiss, Arthur et al. (2004) T cell receptor engagement leads to phosphorylation of clathrin heavy chain during receptor internalization. J Exp Med 199:981-91
Pando, Marcelo J; Gardiner, Clair M; Gleimer, Michael et al. (2003) The protein made from a common allele of KIR3DL1 (3DL1*004) is poorly expressed at cell surfaces due to substitution at positions 86 in Ig domain 0 and 182 in Ig domain 1. J Immunol 171:6640-9
Shilling, Heather G; Guethlein, Lisbeth A; Cheng, Nathalie W et al. (2002) Allelic polymorphism synergizes with variable gene content to individualize human KIR genotype. J Immunol 168:2307-15
Khakoo, Salim I; Geller, Ron; Shin, Sunny et al. (2002) The D0 domain of KIR3D acts as a major histocompatibility complex class I binding enhancer. J Exp Med 196:911-21
Chen, Liguang; Widhopf, George; Huynh, Lang et al. (2002) Expression of ZAP-70 is associated with increased B-cell receptor signaling in chronic lymphocytic leukemia. Blood 100:4609-14
Stoddart, Angela; Dykstra, Michelle L; Brown, Bruce K et al. (2002) Lipid rafts unite signaling cascades with clathrin to regulate BCR internalization. Immunity 17:451-62
Shilling, Heather G; Young, Neil; Guethlein, Lisbeth A et al. (2002) Genetic control of human NK cell repertoire. J Immunol 169:239-47
Bennett, E M; Chen, C Y; Engqvist-Goldstein, A E et al. (2001) Clathrin hub expression dissociates the actin-binding protein Hip1R from coated pits and disrupts their alignment with the actin cytoskeleton. Traffic 2:851-8
Bennett, E M; Lin, S X; Towler, M C et al. (2001) Clathrin hub expression affects early endosome distribution with minimal impact on receptor sorting and recycling. Mol Biol Cell 12:2790-9

Showing the most recent 10 out of 12 publications