ANDREA TENNER

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Extensive innate immune gene activation accompanies brain aging, increasing vulnerability to cognitive decline and neurodegeneration: a microarray study
    David H Cribbs
    Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, 1226 Gillespie NRF, Irvine, CA 92697, USA
    J Neuroinflammation 9:179. 2012
  2. pmc Complement activation fragment C5a receptors, CD88 and C5L2, are associated with neurofibrillary pathology
    Maria I Fonseca
    Dept of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697 3900, USA
    J Neuroinflammation 10:25. 2013
  3. pmc Contribution of complement activation pathways to neuropathology differs among mouse models of Alzheimer's disease
    Maria I Fonseca
    Department of Molecular Biology and Biochemistry, University of California Irvine, CA, USA
    J Neuroinflammation 8:4. 2011
  4. ncbi Membrane receptors for soluble defense collagens
    A J Tenner
    Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697 3900, USA
    Curr Opin Immunol 11:34-41. 1999
  5. ncbi Influence of innate immune responses on autoimmunity
    Andrea J Tenner
    Center for Immunology, University of California, Irvine 3205 McGaugh Hall, Irvine, CA 92697 3900, USA
    Autoimmunity 37:83-4. 2004
  6. ncbi C1qR(P), a myeloid cell receptor in blood, is predominantly expressed on endothelial cells in human tissue
    M I Fonseca
    Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA 92697, USA
    J Leukoc Biol 70:793-800. 2001
  7. ncbi Complement in Alzheimer's disease: opportunities for modulating protective and pathogenic events
    A J Tenner
    Department of Molecular Biology and Biochemistry, 3205 Biological Sciences II, University of California, Irvine 92697 3900, USA
    Neurobiol Aging 22:849-61. 2001
  8. ncbi Human cord blood leukocyte innate immune responses to defense collagens
    Hideki Maruyama
    Department of Pediatrics, University of California, Irvine, CA 92697, USA
    Pediatr Res 54:724-31. 2003
  9. ncbi Cell surface expression of C1qRP/CD93 is stabilized by O-glycosylation
    Minha Park
    Department of Molecular Biology and Biochemistry, University of California, Irvine, California 92697 3900, USA
    J Cell Physiol 196:512-22. 2003
  10. pmc Modulated interaction of the ERM protein, moesin, with CD93
    MingYu Zhang
    Department of Molecular Biology and Biochemistry, Center for Immunology, University of California, Irvine, CA 92697, USA
    Immunology 115:63-73. 2005

Research Grants

  1. COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESIS
    ANDREA TENNER; Fiscal Year: 2007
  2. INTERACTION OF CLQ ON PHAGOCYTIC CELLS
    ANDREA TENNER; Fiscal Year: 2007
  3. INTERACTION OF CLQ ON PHAGOCYTIC CELLS
    Andrea Joan Tenner; Fiscal Year: 2010
  4. INTERACTION OF CLQ ON PHAGOCYTIC CELLS
    ANDREA TENNER; Fiscal Year: 2009
  5. INTERACTION OF CIQ ON PHAGOCYTIC CELLS
    ANDREA TENNER; Fiscal Year: 2004
  6. COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESIS
    ANDREA TENNER; Fiscal Year: 2003
  7. COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESIS
    ANDREA TENNER; Fiscal Year: 1999
  8. INTERACTION OF CLQ ON PHAGOCYTIC CELLS
    ANDREA TENNER; Fiscal Year: 1999
  9. COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESIS
    Andrea Joan Tenner; Fiscal Year: 2010

Collaborators

  • D A Fraser
  • Suzanne S Bohlson
  • Trent M Woodruff
  • June Zhou
  • P M Carpenter
  • F M LaFerla
  • Ming Li
  • Nenoo Rawal
  • Maria I Fonseca
  • Shu Hui Chu
  • Rahasson R Ager
  • David H Cribbs
  • Stephen M Taylor
  • Sam D Sanderson
  • Karntipa Pisalyaput
  • Anna P Lillis
  • MingYu Zhang
  • Maria Isabel Fonseca
  • Minha Park
  • Hideki Maruyama
  • Guenahel H Danet
  • Susan O McGuire
  • Scott E Counts
  • Nicole C Berchtold
  • M I Fonseca
  • Paul D Coleman
  • Joseph Rogers
  • Victoria Perreau
  • Carl W Cotman
  • Marie E Benoit
  • Alisia M Berci
  • Douglas G Peters
  • Yuko Kimura
  • Ozkan Yazan
  • Mallary C Greenlee
  • Irina Mikhailenko
  • Dudley K Strickland
  • Salvatore V Pizzo
  • Marisela Dy
  • Juan C Troncoso
  • Marina Botto
  • Claudia H Kawas
  • Feizal Waffarn
  • Manuel Galvan
  • M Celeste Simon
  • Dominique A Bonnet
  • Gary Butler
  • Jennifer L Luongo
  • Min Min Lu
  • G Palmarini
  • E L Nelson
  • M Park

Detail Information

Publications28

  1. pmc Extensive innate immune gene activation accompanies brain aging, increasing vulnerability to cognitive decline and neurodegeneration: a microarray study
    David H Cribbs
    Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, 1226 Gillespie NRF, Irvine, CA 92697, USA
    J Neuroinflammation 9:179. 2012
    ..This study undertakes a systematic and comprehensive analysis of brain gene expression profiles of immune/inflammation-related genes in aging and Alzheimer's disease (AD)...
  2. pmc Complement activation fragment C5a receptors, CD88 and C5L2, are associated with neurofibrillary pathology
    Maria I Fonseca
    Dept of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697 3900, USA
    J Neuroinflammation 10:25. 2013
    ..Previously, we reported that a CD88 specific antagonist (PMX205) decreased the pathology and improved cognition in transgenic models of AD suggesting that C5a/C5aR interaction has an important role in the progression of the disease...
  3. pmc Contribution of complement activation pathways to neuropathology differs among mouse models of Alzheimer's disease
    Maria I Fonseca
    Department of Molecular Biology and Biochemistry, University of California Irvine, CA, USA
    J Neuroinflammation 8:4. 2011
    ....
  4. ncbi Membrane receptors for soluble defense collagens
    A J Tenner
    Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697 3900, USA
    Curr Opin Immunol 11:34-41. 1999
    ....
  5. ncbi Influence of innate immune responses on autoimmunity
    Andrea J Tenner
    Center for Immunology, University of California, Irvine 3205 McGaugh Hall, Irvine, CA 92697 3900, USA
    Autoimmunity 37:83-4. 2004
  6. ncbi C1qR(P), a myeloid cell receptor in blood, is predominantly expressed on endothelial cells in human tissue
    M I Fonseca
    Department of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, CA 92697, USA
    J Leukoc Biol 70:793-800. 2001
    ..The predominant presence of C1qR(P) in endothelial cells, while compatible with a phagocytic role in host defense and/or clearance of cellular material, suggests other possible novel roles for this receptor...
  7. ncbi Complement in Alzheimer's disease: opportunities for modulating protective and pathogenic events
    A J Tenner
    Department of Molecular Biology and Biochemistry, 3205 Biological Sciences II, University of California, Irvine 92697 3900, USA
    Neurobiol Aging 22:849-61. 2001
    ....
  8. ncbi Human cord blood leukocyte innate immune responses to defense collagens
    Hideki Maruyama
    Department of Pediatrics, University of California, Irvine, CA 92697, USA
    Pediatr Res 54:724-31. 2003
    ..We also confirm that C1q and MBL are present in neonate circulation. Thus, the data demonstrate that these recognition and effector mechanisms of the innate system are functional in the newborn and similar to that of adult cells...
  9. ncbi Cell surface expression of C1qRP/CD93 is stabilized by O-glycosylation
    Minha Park
    Department of Molecular Biology and Biochemistry, University of California, Irvine, California 92697 3900, USA
    J Cell Physiol 196:512-22. 2003
    ..These studies demonstrate that O-glycosylation is important in the stable cell surface expression of C1qRP/CD93 ...
  10. pmc Modulated interaction of the ERM protein, moesin, with CD93
    MingYu Zhang
    Department of Molecular Biology and Biochemistry, Center for Immunology, University of California, Irvine, CA 92697, USA
    Immunology 115:63-73. 2005
    ....
  11. ncbi C1q and MBL, components of the innate immune system, influence monocyte cytokine expression
    Deborah A Fraser
    Department of Molecular Biology, University of California, Irvine, 92697, USA
    J Leukoc Biol 80:107-16. 2006
    ..These data support the hypothesis that defense collagen-mediated suppression of a proinflammatory response may be an important step in the avoidance of autoimmunity during the clearance of apoptotic cells...
  12. pmc C1q enhances microglial clearance of apoptotic neurons and neuronal blebs, and modulates subsequent inflammatory cytokine production
    Deborah A Fraser
    Department of Molecular Biology and Biochemistry, University of California, Irvine, California 92697 3900, USA
    J Neurochem 112:733-43. 2010
    ..The data are consistent with a protective role for C1q in the CNS during early stages of cell death by enhancing microglial clearance of apoptotic cells and suppressing proinflammatory cytokines...
  13. pmc Innate immune proteins C1q and mannan-binding lectin enhance clearance of atherogenic lipoproteins by human monocytes and macrophages
    Deborah A Fraser
    Department of Molecular Biology and Biochemistry, Institute for Immunology, University of California, Irvine, CA 92697, USA
    J Immunol 185:3932-9. 2010
    ..These results suggest a novel pathway in which C1q and MBL influence removal and metabolism of atherogenic forms of LDL in the early stages of atherosclerosis...
  14. ncbi CD93 is rapidly shed from the surface of human myeloid cells and the soluble form is detected in human plasma
    Suzanne S Bohlson
    Department of Molecular Biology and Biochemistry, Center for Immunology, University of California Irvine, 2419 McGaugh Hall, Irvine, CA 92697, USA
    J Immunol 175:1239-47. 2005
    ....
  15. ncbi CD93 interacts with the PDZ domain-containing adaptor protein GIPC: implications in the modulation of phagocytosis
    Suzanne S Bohlson
    Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697, USA
    J Leukoc Biol 77:80-9. 2005
    ..These protein interactions may participate as molecular switches in modulating cellular phagocytic activity...
  16. pmc C1q differentially modulates phagocytosis and cytokine responses during ingestion of apoptotic cells by human monocytes, macrophages, and dendritic cells
    Deborah A Fraser
    Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697 3900, USA
    J Immunol 183:6175-85. 2009
    ....
  17. pmc Microglial C5aR (CD88) expression correlates with amyloid-beta deposition in murine models of Alzheimer's disease
    Rahasson R Ager
    Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697 3900, USA
    J Neurochem 113:389-401. 2010
    ..This further supports the targeted inhibition of specific complement mediated activities as an approach for AD therapy...
  18. ncbi Generation of inhibitory NFkappaB complexes and phosphorylated cAMP response element-binding protein correlates with the anti-inflammatory activity of complement protein C1q in human monocytes
    Deborah A Fraser
    Department of Molecular Biology and Biochemistry, Center for Immunology, University of California, Irvine, California 92697, USA
    J Biol Chem 282:7360-7. 2007
    ..Because C1q and other defense collagens have been shown to enhance clearance of apoptotic cells, this regulatory pathway may be beneficial in avoiding autoimmunity and/or resolving inflammation...
  19. ncbi Complement proteins C1q and MBL are pattern recognition molecules that signal immediate and long-term protective immune functions
    Suzanne S Bohlson
    Department of Molecular Biology and Biochemistry, Center for Immunology, University of California, Irvine, CA 92697, USA
    Mol Immunol 44:33-43. 2007
    ....
  20. pmc Complement C3 and C4 expression in C1q sufficient and deficient mouse models of Alzheimer's disease
    Jun Zhou
    Department of Molecular Biology and Biochemistry, Institute for Brain Aging and Dementia, Center for Immunology, University of California, Irvine, California 92697 3900, USA
    J Neurochem 106:2080-92. 2008
    ..Finally, induced expression of C3 in a subset of astrocytes suggests the existence of differential activation states of these cells...
  21. doi Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's disease
    Maria I Fonseca
    Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697, USA
    J Immunol 183:1375-83. 2009
    ..e., C5aR) can interfere with neuroinflammation and neurodegeneration in AD rodent models, suggesting a novel therapeutic target for reducing pathology and improving cognitive function in human AD patients...
  22. ncbi Absence of C1q leads to less neuropathology in transgenic mouse models of Alzheimer's disease
    Maria Isabel Fonseca
    Department of Molecular Biology and Biochemistry, University of California, Irvine, California 92697, USA
    J Neurosci 24:6457-65. 2004
    ....
  23. ncbi Neuronal localization of C1q in preclinical Alzheimer's disease
    Maria I Fonseca
    Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697, USA
    Neurobiol Dis 15:40-6. 2004
    ..Thus, it is possible that this neuronal-associated C1q reflects an early, but transient, response to injury that may modulate the progression of neurological dysfunction in AD...
  24. ncbi The double-edged flower: roles of complement protein C1q in neurodegenerative diseases
    Andrea J Tenner
    Department of Molecular Biology, Center for Immunology, University of California, Irvine, CA 92697, USA
    Adv Exp Med Biol 586:153-76. 2006
    ..Rather, strategies that enhance or mimic the protective effects of C1q as well as strategies that inhibit the detrimental processes should be fully investigated...
  25. pmc Development of a humanized C1q A chain knock-in mouse: assessment of antibody independent beta-amyloid induced complement activation
    Ming Li
    Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697, USA
    Mol Immunol 45:3244-52. 2008
    ..The humanized C1q mouse generated here should provide a better animal model for assessing the mechanisms of C1 activation and the contribution of C1q to human health and disease...
  26. ncbi Complement component C1q inhibits beta-amyloid- and serum amyloid P-induced neurotoxicity via caspase- and calpain-independent mechanisms
    Karntipa Pisalyaput
    Department of Molecular Biology and Biochemistry, Institute for Brain Aging and Dementia, Center for Immunology, University of California, Irvine, California 92697, USA
    J Neurochem 104:696-707. 2008
    ..These data support a neuroprotective role for C1q which should be further investigated to uncover mechanisms which may be therapeutically targeted to slow neurodegeneration via direct inhibition of neuronal loss...
  27. pmc C1qRp defines a new human stem cell population with hematopoietic and hepatic potential
    Guenahel H Danet
    Howard Hughes Medical Institute and Abramson Family Cancer Research Institute, Molecular Cardiology Research Center, University of Pennsylvania School of Medicine, BRB 2 3, 421 Curie Boulevard, Philadelphia, PA 19104 6160, USA
    Proc Natl Acad Sci U S A 99:10441-5. 2002
    ..These findings may have important scientific and clinical implications in the field of human stem cell biology and transplantation...
  28. pmc Murine low-density lipoprotein receptor-related protein 1 (LRP) is required for phagocytosis of targets bearing LRP ligands but is not required for C1q-triggered enhancement of phagocytosis
    Anna P Lillis
    Center for Vascular and Inflammatory Diseases and Department of Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Immunol 181:364-73. 2008
    ....

Research Grants27

  1. COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESIS
    ANDREA TENNER; Fiscal Year: 2007
    ..abstract_text> ..
  2. INTERACTION OF CLQ ON PHAGOCYTIC CELLS
    ANDREA TENNER; Fiscal Year: 2007
    ..abstract_text> ..
  3. INTERACTION OF CLQ ON PHAGOCYTIC CELLS
    Andrea Joan Tenner; Fiscal Year: 2010
    ....
  4. INTERACTION OF CLQ ON PHAGOCYTIC CELLS
    ANDREA TENNER; Fiscal Year: 2009
    ....
  5. INTERACTION OF CIQ ON PHAGOCYTIC CELLS
    ANDREA TENNER; Fiscal Year: 2004
    ....
  6. COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESIS
    ANDREA TENNER; Fiscal Year: 2003
    ..Since complement has been implicated in a number of other neurodegenerative diseases, it is likely that the investigators' findings will be relevant to other diseases as well. ..
  7. COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESIS
    ANDREA TENNER; Fiscal Year: 1999
    ..Finally, the development of the in vitro model described here will allow testing of potential drugs that may modulate deleterious activities in an effort to slow or stop progression of this disease. ..
  8. INTERACTION OF CLQ ON PHAGOCYTIC CELLS
    ANDREA TENNER; Fiscal Year: 1999
    ..The research proposed here will provide necessary information for future development of therapeutic strategies for these conditions and other immunodeficient states. ..
  9. COMPLEMENT AND INFLAMMATORY FACTORS IN AD PATHOGENESIS
    Andrea Joan Tenner; Fiscal Year: 2010
    ....