Linda Curtiss

Summary

Affiliation: The Scripps Research Institute
Country: USA

Publications

  1. ncbi Participation of innate and acquired immunity in atherosclerosis
    L K Curtiss
    Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA
    Immunol Res 21:167-76. 2000
  2. ncbi Apolipoprotein E and atherosclerosis
    L K Curtiss
    The Scripps Research Institute, Department of Immunology, La Jolla, California 92037, USA
    Curr Opin Lipidol 11:243-51. 2000
  3. ncbi Emerging role of Toll-like receptors in atherosclerosis
    Linda K Curtiss
    Department of Immunology and Microbial Science, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    J Lipid Res 50:S340-5. 2009
  4. ncbi The toll of Toll-like receptors, especially toll-like receptor 2, on murine atherosclerosis
    L K Curtiss
    The Scripps Research Institute, Department of Immunology, IMM 17, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Curr Drug Targets 8:1230-8. 2007
  5. ncbi What is so special about apolipoprotein AI in reverse cholesterol transport?
    Linda K Curtiss
    Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA
    Arterioscler Thromb Vasc Biol 26:12-9. 2006
  6. ncbi Increased endothelial expression of Toll-like receptor 2 at sites of disturbed blood flow exacerbates early atherogenic events
    Adam E Mullick
    Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA
    J Exp Med 205:373-83. 2008
  7. ncbi Atherosclerosis in mice is not affected by a reduction in tissue factor expression
    Rachel E Tilley
    Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
    Arterioscler Thromb Vasc Biol 26:555-62. 2006
  8. ncbi Inflammation in atherosclerosis: lesion formation in LDL receptor-deficient mice with perforin and Lyst(beige) mutations
    Natalie K Schiller
    Scripps Research Institute, Department of Immunology, La Jolla, Calif, USA
    Arterioscler Thromb Vasc Biol 22:1341-6. 2002
  9. ncbi Atheroprotective potential of macrophage-derived phospholipid transfer protein in low-density lipoprotein receptor-deficient mice is overcome by apolipoprotein AI overexpression
    David T Valenta
    Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
    Arterioscler Thromb Vasc Biol 26:1572-8. 2006
  10. ncbi Transcriptional repression of atherogenic inflammation: modulation by PPARdelta
    Chih Hao Lee
    Howard Hughes Medical Institute, Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA
    Science 302:453-7. 2003

Research Grants

  1. IMMUNOBIOLOGY OF APOLIPOPROTEIN E
    Linda Curtiss; Fiscal Year: 2002
  2. IMMUNOCHEMICAL STRUCTURE FUNCTION OF APOLIPOPROTEIN A-I
    Linda Curtiss; Fiscal Year: 2003
  3. Atherosclerosis in Beige(Lyst) Mutant
    Linda Curtiss; Fiscal Year: 2006
  4. Blood System in Coagulation and Vessel Disease
    Linda Curtiss; Fiscal Year: 2007
  5. Toll Receptors in Atherosclerosis
    Linda Curtiss; Fiscal Year: 2007
  6. IMMUNOCHEMICAL STRUCTURE/FUNCTION OF APOLIPOPROTEIN A-I
    Linda Curtiss; Fiscal Year: 2007
  7. IMMUNOCHEMICAL STRUCTURE/FUNCTION OF APOLIPOPROTEIN AI
    Linda Curtiss; Fiscal Year: 1999
  8. IMMUNOBIOLOGY OF APOLIPOPROTEIN E
    Linda Curtiss; Fiscal Year: 1993
  9. IMMUNOCHEMICAL STRUCTURE/FUNCTION OF APOLIPOPROTEIN A-I
    Linda Curtiss; Fiscal Year: 1993

Collaborators

Detail Information

Publications32

  1. ncbi Participation of innate and acquired immunity in atherosclerosis
    L K Curtiss
    Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA
    Immunol Res 21:167-76. 2000
    ..By using mouse models of hyperlipidemia, our laboratory is addressing in vivo the participation of both innate inflammatory responses and acquired immune responses in atherosclerosis...
  2. ncbi Apolipoprotein E and atherosclerosis
    L K Curtiss
    The Scripps Research Institute, Department of Immunology, La Jolla, California 92037, USA
    Curr Opin Lipidol 11:243-51. 2000
    ..Third, lesion apolipoprotein E directly modifies both macrophage- and T lymphocyte-mediated immune responses that contribute to this chronic inflammatory disease...
  3. ncbi Emerging role of Toll-like receptors in atherosclerosis
    Linda K Curtiss
    Department of Immunology and Microbial Science, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    J Lipid Res 50:S340-5. 2009
    ..TLR2- and 4-expression exert an overall proatherogenic effect in hyperlipidemic mice. TLR activation of the endothelium promotes lipid accumulation and leukocyte accumulation within lesions...
  4. ncbi The toll of Toll-like receptors, especially toll-like receptor 2, on murine atherosclerosis
    L K Curtiss
    The Scripps Research Institute, Department of Immunology, IMM 17, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Curr Drug Targets 8:1230-8. 2007
    ..Thus, TLR2-mediated cell activation in response to endogenous and exogenous agents is proatherogenic in hyperlipidemic mice...
  5. ncbi What is so special about apolipoprotein AI in reverse cholesterol transport?
    Linda K Curtiss
    Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA
    Arterioscler Thromb Vasc Biol 26:12-9. 2006
    ....
  6. ncbi Increased endothelial expression of Toll-like receptor 2 at sites of disturbed blood flow exacerbates early atherogenic events
    Adam E Mullick
    Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA
    J Exp Med 205:373-83. 2008
    ..This is the first report of in vivo site-specific expression of endothelial cell TLR2. Expression of this receptor on endothelial cells contributed to early atherosclerotic processes in lesion-prone areas of the mouse aorta...
  7. ncbi Atherosclerosis in mice is not affected by a reduction in tissue factor expression
    Rachel E Tilley
    Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
    Arterioscler Thromb Vasc Biol 26:555-62. 2006
    ..To determine whether tissue factor (TF) contributes to the progression of atherosclerotic lesions in mice...
  8. ncbi Inflammation in atherosclerosis: lesion formation in LDL receptor-deficient mice with perforin and Lyst(beige) mutations
    Natalie K Schiller
    Scripps Research Institute, Department of Immunology, La Jolla, Calif, USA
    Arterioscler Thromb Vasc Biol 22:1341-6. 2002
    ....
  9. ncbi Atheroprotective potential of macrophage-derived phospholipid transfer protein in low-density lipoprotein receptor-deficient mice is overcome by apolipoprotein AI overexpression
    David T Valenta
    Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
    Arterioscler Thromb Vasc Biol 26:1572-8. 2006
    ..The atheroprotective properties of macrophage-derived PLTP were not observable in the presence of elevated plasma concentrations of apoAI...
  10. ncbi Transcriptional repression of atherogenic inflammation: modulation by PPARdelta
    Chih Hao Lee
    Howard Hughes Medical Institute, Gene Expression Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA
    Science 302:453-7. 2003
    ..PPARdelta and its ligands may thus serve as therapeutic targets to attenuate inflammation and slow the progression of atherosclerosis...
  11. ncbi Leukocyte-derived hepatic lipase increases HDL and decreases en face aortic atherosclerosis in LDLr-/- mice expressing CETP
    Neil J Hime
    Department of Immunology, The Scripps Research Institute, La Jolla, California, USA
    J Lipid Res 49:2113-23. 2008
    ..Thus, leukocyte-derived HL in CETPtgLDLr(-/-) mice has an atheroprotective role that may involve increased HDL levels...
  12. ncbi DNA vaccination against VEGF receptor 2 reduces atherosclerosis in LDL receptor-deficient mice
    Ramona J Petrovan
    The Scripps Research Institute, Department of Immunology, IMM 17, 10550 North Torrey Pines Rd, La Jolla, CA 92037, USA
    Arterioscler Thromb Vasc Biol 27:1095-100. 2007
    ....
  13. ncbi Macrophage PLTP is atheroprotective in LDLr-deficient mice with systemic PLTP deficiency
    David T Valenta
    Department of Immunology, Scripps Research Institute, La Jolla, CA 92037, USA
    J Lipid Res 49:24-32. 2008
    ..Thus, unlike total systemic PLTP, locally produced macrophage-derived PLTP beneficially alters lipoprotein metabolism and reduces lesion progression in hyperlipidemic mice...
  14. ncbi Expression of the Lyst(beige) mutation is atheroprotective in chow-fed apolipoprotein E-deficient mice
    Ramona J Petrovan
    Department of Immunology, Scripps Research Institute, La Jolla, CA 92037, USA
    J Lipid Res 49:429-37. 2008
    ..Thus, expression of the beige mutation in all cell types involved in lesion development contributed to atheroprotection in chow-fed ApoE(-/-) mice...
  15. ncbi Modulation of atherosclerosis in mice by Toll-like receptor 2
    Adam E Mullick
    Department of Immunology, The Scripps Research Institute, La Jolla, California 92037, USA
    J Clin Invest 115:3149-56. 2005
    ..These studies support the concept that chronic or recurrent microbial infections may contribute to atherosclerotic disease. Additionally, these data suggest the presence of host-derived endogenous TLR2 agonists...
  16. ncbi TLR2 in murine atherosclerosis
    Peter S Tobias
    Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA
    Semin Immunopathol 30:23-7. 2008
    ..It does involve lipid accumulation, but inflammation appears to be an important driving factor. Consequently, our laboratory undertook to examine the role(s) of TLRs, and especially TLR2, in murine models of atherosclerosis...
  17. ncbi Toll-like receptors and atherosclerosis: key contributors in disease and health?
    Adam E Mullick
    Department of Immunology, The Scripps Research Institute, La Jolla, CA, 92037, USA
    Immunol Res 34:193-209. 2006
    ..Finally, an appreciation of the pro- and anti-atherosclerotic mechanisms of TLR activation over the entire lifetime of an organism will provide clues to the role of TLRs in both health and disease...
  18. ncbi Overexpression of human ApoAI transgene provides long-term atheroprotection in LDL receptor-deficient mice
    David T Valenta
    Department of Immunology, The Scripps Research Institute, 10550 North Torrey, Pines Road, La Jolla, CA 92037, USA
    Atherosclerosis 189:255-63. 2006
    ..This was observed without a change in total HDL cholesterol levels. Thus, elevated levels of human apoAI in LDL receptor-deficient mice lacking mouse apoAI conferred profound protection against diet-induced over extended periods of time...
  19. ncbi Participation of macrophages in atherosclerotic lesion morphology in LDLr-/- mice
    Natalie K Schiller
    The Scripps Research Institute, Department of Immunology, La Jolla, CA 92037, USA
    J Lipid Res 45:1398-409. 2004
    ..These results suggested that impaired macrophage function by itself did not account for the stable lesion morphology of beige,LDLr-/- double-mutant mice...
  20. ncbi Up-regulated expression of the CXCR2 ligand KC/GRO-alpha in atherosclerotic lesions plays a central role in macrophage accumulation and lesion progression
    William A Boisvert
    Department of Immunology, The Scripps Research Institute, La Jolla, California, USA
    Am J Pathol 168:1385-95. 2006
    ....
  21. ncbi PPARdelta regulates multiple proinflammatory pathways to suppress atherosclerosis
    Grant D Barish
    Howard Hughes Medical Institute, Gene Expression Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 105:4271-6. 2008
    ..These results reveal that PPARdelta antagonizes multiple proinflammatory pathways and suggest PPARdelta-selective drugs as candidate therapeutics for atherosclerosis...
  22. ncbi Phospholipid transfer protein is present in human atherosclerotic lesions and is expressed by macrophages and foam cells
    Catherine M Desrumaux
    Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA
    J Lipid Res 44:1453-61. 2003
    ..7 cells as well. Thus, this study demonstrates that PLTP is expressed by macrophages, is regulated by cholesterol loading, and is present in atherosclerotic lesions...
  23. ncbi Disruption of tissue-specific fucosyltransferase VII, an enzyme necessary for selectin ligand synthesis, suppresses atherosclerosis in mice
    Jonathan M Gitlin
    Department of Immunology, The Scripps Research Institute, La Jolla, California, USA
    Am J Pathol 174:343-50. 2009
    ..These studies indicate that selectin ligands, particularly those for E- and P-selectins, play an important role in the pathogenesis of atherosclerosis by regulating macrophage accumulation in atherosclerotic lesions...
  24. ncbi Adiposity, dyslipidemia, and insulin resistance in mice with targeted deletion of phospholipid scramblase 3 (PLSCR3)
    Therese Wiedmer
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 101:13296-301. 2004
    ....
  25. ncbi IL-5 links adaptive and natural immunity specific for epitopes of oxidized LDL and protects from atherosclerosis
    Christoph J Binder
    Division of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla 92093 0682, USA
    J Clin Invest 114:427-37. 2004
    ..Thus, IL-5 links adaptive and natural immunity specific to epitopes of OxLDL and protects from atherosclerosis, in part by stimulating the expansion of atheroprotective natural IgM specific for OxLDL...
  26. ncbi Overexpression of interleukin-10 by activated T lymphocytes inhibits atherosclerosis in LDL receptor-deficient Mice by altering lymphocyte and macrophage phenotypes
    Laura J Pinderski
    Department of Medicine, University of California Los Angeles, USA
    Circ Res 90:1064-71. 2002
    ..These studies demonstrate that T lymphocyte IL-10 can influence the function of other immune cells to reduce the development of advanced atherosclerotic lesions in mice...
  27. ncbi Is two out of three enough for ABCG1?
    Linda K Curtiss
    Arterioscler Thromb Vasc Biol 26:2175-7. 2006
  28. ncbi Facilitated replacement of Kupffer cells expressing a paraoxonase-1 transgene is essential for ameliorating atherosclerosis in mice
    Gary Bradshaw
    Department of Biology and Heart Institute, San Diego State University, San Diego, CA 92182, USA
    Proc Natl Acad Sci U S A 102:11029-34. 2005
    ..GdCl(3)-facilated replacement of Kupffer cells may enhance the efficacy of other HSC-based gene therapies...
  29. ncbi Apolipoprotein A-II inhibits high density lipoprotein remodeling and lipid-poor apolipoprotein A-I formation
    Kerry Anne Rye
    Lipid Research Laboratory, Hanson Institute, Adelaide, South Australia 5000, Australia
    J Biol Chem 278:22530-6. 2003
    ....
  30. ncbi Evidence that phospholipids play a key role in pre-beta apoA-I formation and high-density lipoprotein remodeling
    Kerry Anne Rye
    Lipid Research Laboratory, Hanson Institute, Adelaide, South Australia, Australia 5000
    Biochemistry 41:12538-45. 2002
    ..In conclusion, these results show that phospholipids play a key role in the CETP-mediated remodeling of rHDL and pre-beta apoA-I formation...
  31. ncbi Regulated expression of the apolipoprotein E/C-I/C-IV/C-II gene cluster in murine and human macrophages. A critical role for nuclear liver X receptors alpha and beta
    Puiying A Mak
    Department of Biological Chemistry and Medicine, University of California, Los Angeles, California 90095, USA
    J Biol Chem 277:31900-8. 2002
    ..These results suggest an alternative mechanism by which lipids are removed from macrophage foam cells...
  32. ncbi Thematic review series: The immune system and atherogenesis. Paying the price for pathogen protection: toll receptors in atherogenesis
    Peter Tobias
    Department of Immunology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    J Lipid Res 46:404-11. 2005
    ..In this review, we discuss our current understanding of the role of TLRs and their coactivators in atherosclerosis, with particular emphasis on studies in atherosclerosis-prone hypercholesterolemic mice...

Research Grants35

  1. IMMUNOBIOLOGY OF APOLIPOPROTEIN E
    Linda Curtiss; Fiscal Year: 2002
    ..abstract_text> ..
  2. IMMUNOCHEMICAL STRUCTURE FUNCTION OF APOLIPOPROTEIN A-I
    Linda Curtiss; Fiscal Year: 2003
    ..abstract_text> ..
  3. Atherosclerosis in Beige(Lyst) Mutant
    Linda Curtiss; Fiscal Year: 2006
    ..The power of comparing LDLr- /-bg with LDLr-/- mice will allow us to focus on those cellular activities that are physiologically relevant and participate in vivo in a very complex and still poorly understood disease process. ..
  4. Blood System in Coagulation and Vessel Disease
    Linda Curtiss; Fiscal Year: 2007
    ..End of Abstract) ..
  5. Toll Receptors in Atherosclerosis
    Linda Curtiss; Fiscal Year: 2007
    ..These studies will enhance our understanding of inflammatory responses in atherosclerosis and potentially identify new TLR targets for therapeutic intervention to reverse or reduce disease risk. ..
  6. IMMUNOCHEMICAL STRUCTURE/FUNCTION OF APOLIPOPROTEIN A-I
    Linda Curtiss; Fiscal Year: 2007
    ..We propose that core lipid reduction by triglyceride hydrolysis and remodeling by PLTP and CETP release lipid-poor apoAI from HDL to facilitate efflux from Mphi foam cells within atherosclerotic lesions. ..
  7. IMMUNOCHEMICAL STRUCTURE/FUNCTION OF APOLIPOPROTEIN AI
    Linda Curtiss; Fiscal Year: 1999
    ....
  8. IMMUNOBIOLOGY OF APOLIPOPROTEIN E
    Linda Curtiss; Fiscal Year: 1993
    ..Finally, the structural regions of apo E that are responsible for its inhibitory activity will be identified using monoclonal antibodies and synthetic peptides...
  9. IMMUNOCHEMICAL STRUCTURE/FUNCTION OF APOLIPOPROTEIN A-I
    Linda Curtiss; Fiscal Year: 1993
    ....