Andrea J. Tenner

University of California

3205 McGaugh Hall
2228 McGaugh Hall
Mail Code: 3900
Irvine, CA 92697

PHONE: (949) 824-3268
FAX: (949) 824-8551



Andrea J. Tenner
Professor, Molecular Biology and Biochemistry
School of Biological Sciences
Professor, Pathology
School of Medicine
Professor, Neurobiology and Behavior
School of Biological Sciences
Member, Institute for Memory Impairments and Neurological Disorders (UCI MIND)
Research Centers and Institutes
Member, Institute for Immunology
Research Centers and Institutes

PH.D., University of California, San Diego, 1977

Research Interests
Neuronflammation; Complement; Alzheimer's Disease; Innate Immunity; Phagocytosis

Faculty/lab web:
Faculty/lab web:
Graduate Programs:
Immunology and Pathogenesis Cellular and Molecular Biosciences Interdepartmental Neuroscience Program
Professional Society American Association of Immunology Society for Neuroscience American Society for Cell Biology International Complement Society, Founding Councilor Society for Leukocyte Biology American Society for Neurochemistry American Society for Biochemistry and Molecular Biology International Complement Society, Past President ISTAART – Vice Chair, PIA Immunity and Neurodegeneration
The basic understanding of the immune system has undergone a substantial paradigm shift in the past decade as an awareness of the power and influence of the innate immune system has emerged. Essentially, it is now being recognized that the nature of the first response to invasion has significant influence in determining the nature of the subsequent adaptive immune response. That is, it is this first response that assesses the level of danger of a particular intrusion or injury and initiates a program of protection.

My laboratory is focused on the role of specific elements of the innate immune system in host defense and in maintaining a balance of protective responses in the host. We have been elucidating mechanisms by which phagocytic cells regulate induction of an appropriate adaptive response. As phagocytic cells ingest distinct particles specific gene expression programs are initiated that influences th induction of an appropriate immune response. Thus, we are investigating the down stream events such as cytokine expression resulting from the interaction of pattern recognition signals in the context of various particles targeted for ingestion.

The second major research area is the investigation of the role of complement activation and subsequent inflammation in Alzheimer’s Disease. The neuropathological structures that are the hallmark of Alzheimer's disease (AD) include senile plaques composed of a proposed pathogenic peptide fragment, beta-amyloid (A-Beta), neurofibrillary tangles and loss of neurons. Using mouse models of AD, we have evidence consistent with the hypothesis that complement activation and subsequent inflammatory events contribute to the pathogenesis of dementia in AD, and are currently testing candidate therapeutics to prevent or slow the progression of pathogenic events that lead to Alzheimer’s Disease in mouse models. In addition, we postulate that C1q may be a response to injury that could play a protective role in the early stages of disease by enhancing the clearance of cellular debris, altering the effects of the amyloid peptide on microglia, and/or providing direct neuroprotective effects. We use novel mouse models and cell isolation procedures to assess the molecular basis of these effects to identify targets for therapeutic intervention in neurodegenerative diseases. Patents: "Host Defense Enhancement", Andrea J. Tenner and Ronald R. Nepomuceno, filed November 18, 1996, issued October 12, 1999. U.S. Patent # 5,965,439.

Other Experience
ADVANCE Equity Advisor, UCI, 2004—2007

Updated: Last Updated: 09/10/2018

  Hernandez, M.X., Jiang, S. Cole,T.A., Chu, S-H, Fonseca, M.I., Fang, M.J., Hohsfield, L.A., Torres, M.D., Green, K.N., Wetsel, R.A., Mortazavi,A. and Tenner, A.J. Prevention of C5aR1 Signaling Delays Microglial Inflammatory Polarization, Favors Clearance Pathways and Suppresses Cognitive Loss, Mol. Neurodegeneration, 12:66, 2017. PMC5604420

Thielens, N.M., Tedesco, F., Bohlson,S.S., Gaboriaud,C., Tenner, A.J. C1q: A fresh look upon an old molecule. Mol. Immunol. 89 :73-83, 2017

Crane, A., Brubaker, W.D., Johansson, J.U., Trigunaite, A., Ceballos, J., Bradt, B., Glavis-Bloom, C., Wallace, T.L., Tenner, A.J., and Rogers,J. Peripheral complement interactions with amyloid ß peptide (Aß) in Alzheimer's disease: 2. Relationship to Aß immunotherapy, Alzheimer’s and Dementia, 10.1016/j.jalz.2017.04.015, 2017.

Brubaker, W.D., Crane, A., Johansson, J.U., Yen, K., Garfinkel, K., Mastroeni,D, Leonard, B.,Asok, P., Bradt,B., Sabbagh,M., Wallace, T.L., Glavis-Bloom, C., Tenner, A.J., and Rogers,J., Peripheral complement interactions with amyloid ß peptide (Aß) in Alzheimer’s disease: 1. Erythrocyte clearance of Aß. Alzheimer’s and Dementia, 2017. PMID: 28475854 DOI:10.1016/j.jalz.2017.03.010

Current publications from Pubmed

Hernandez, M.X., Namiranian,P., Nguyen, E., Fonseca, M.I., and Tenner, A.J. C5a increases the injury to primary neurons elicited by fibrillar amyloid beta. ASNeuro DOI: 10.1177/1759091416687871, 2017. PMID:28078911

Fonseca, M.I., Chu,S-H., Hernandez, M.X., Fang, M.J., Modarresi, L., Selvan, P., MacGregor G.R. and Tenner, A.J., Cell specific deletion of C1qa identifies microglia as the dominant source of C1q in mouse brain J. Neuroinflammation, 14:48, 2017.

Fonseca, M.I., Chu,S-H., Pierce, A.L., Brubaker, W.D., Hauhart, R.E., Mastroeni, D., Clarke, E.V., Rogers, J., Atkinson, J.P., and Tenner, A.J., Analysis of the putative role of CR1 in Alzheimer’s disease: Genetic association, expression, and function. Plos One 11(2): e0149792 , 2016. (PMCID: PMC4767815)

Clarke, E.V., Weist, B.M., Walsh, C.M. and Tenner, A.J., Complement protein C1q bound to apoptotic cells suppresses human macrophage and dendritic-cell mediated Th17 and Th1 T cell subset proliferation. J. Leuk. Biol. 97:147-160, 2015.

Clarke, E.V. and Tenner, A.J., Complement modulation of T cell immune responses during homeostasis and disease. J. Leuk. Biol. 96:745-756, 2014.

Benoit, M.E., Hernandez, M., Dinh, M., Benavente,F., Vasquez,O. and Tenner, A.J. C1q-induced LRP1B and GPR6, expressed early in AD mouse models, are essential for the C1q-mediated protection against Aß neurotoxicity, J. Biol. Chem. 288:654-665 2013. PMC3537064

Fonseca, M.I., McGuire, S.O., Counts,S.E. and Tenner, A.J., Complement Activation Fragment C5a Receptors, CD88 and C5L2, are associated with neurofibrillary pathology. J. Neuroinflammation 10:25, 2013. PMCID: PMC3605123

Chandrasekhar, A., Dinasarapu,D.R., Tenner, A.J., Subramaniam, S., Complement C1q subcomponent subunit A, UCSD Molecule Page, 2012, doi:10.6072/H0.MP.A004228.01)

Benoit, M.E., Clarke, E.V., Morgado, P., Fraser, D.A. and Tenner, A.J., Complement protein C1q directs macrophage polarization and limits inflammasome activity during the uptake of apoptotic cells, J. Immunol 188 5682-5693, 2012.

Linnartz B, Kopatz J, Tenner AJ, Neumann H., Sialic Acid on the neuronal glycocalyx prevents complement c1 binding and complement receptor-3-mediated removal by microglia.
J Neurosci. 32(3):946-52, 2012.

Benoit ME, Tenner AJ., Complement protein C1q-mediated neuroprotection is correlated with regulation of neuronal gene and microRNA expression. J Neurosci. 2011 Mar 2;31(9):3459-69.

Veerhuis R, Nielsen HM, Tenner AJ. Complement in the brain.
Mol Immunol. 2011 Aug;48(14):1592-603.

Fonseca MI, Chu SH, Berci AM, Benoit ME, Peters DG, Kimura Y, Tenner AJ., Contribution of complement activation pathways to neuropathology differs among mouse models of Alzheimer's disease. J Neuroinflammation. 2011 Jan 15;8(1):4.

Fraser D.A., Tenner AJ., Innate immune proteins C1q and mannan-binding lectin enhance clearance of atherogenic lipoproteins by human monocytes and macrophages. J Immunol. 2010 Oct 1;185(7):3932-9.

Fraser.D.A., Pisalyaput, K., and Tenner, A.J., C1q enhances microglial clearance of apoptotic neurons and neuronal blebs, and modulates subsequent inflammatory cytokine production. J. Neurochem. 112:733-743, 2010.

Ager, R.R., Fonseca, M.I., Chu,S., Sanderson, S., Taylor, S.M., Woodruff, T.M., and Tenner, A.J., Microglial C5aR (CD88) expression correlates with amyloid-ß deposition in murine models of Alzheimer’s Disease, J. Neurochem. 113:389–401, 2010.

Klos, A., Tenner, A.J., Johswich, K-O., Ager, R.R., Reis, E.S. and J. Köhl, The Role of the Anaphylatoxins in Health and Disease. Mol. Immunol. 46:13624-13648, 2009.

Fonseca, M.F., Ager, R.R., Chu, S., Yazan, O., Sanderson, S., LaFerla, F.M., Taylor, S.M., Woodruff, T.M., Tenner, A.J., Treatment with a C5aR Antagonist Decreases Pathology and Enhances Behavioral Performance in Murine Models of Alzheimer Disease. J. Immunol. 183:1375-1383, 2009.

Fraser,D.A., Laust, A.K., Nelson, E.L. and Tenner, A.J., C1q differentially modulates phagocytosis and cytokine responses during ingestion of apoptotic cells by human monocytes, macrophages, and dendritic cells. J.Immunol. 183;6175-6185, 2009

Zhou, J., Fonseca,, M.I., Pisalyaput, K. and Tenner, A.J. Complement C3 and C4 expression in murine mouse models of Alzheimer’s Disease. J. Neurochem. 106: 2080-2092, 2008.

Li,M., Ager, R.R., Fraser, D.A., Tjokro, N.O. and Tenner, AJ., Development of a Humanized C1q A Chain Knock-in Mouse: Assessment of Antibody Independent ß-Amyloid Induced Complement Activation. Mol. Immunol. 45:3244-3252, 2008.

Fraser, D.A. and Tenner, A.J. Directing an appropriate immune response: The role of defense collagens and other soluble pattern recognition molecules. Current Drug Targets, "Modulators of the Innate Immune System." Suzanne S. Bohlson, guest editor; Bentham Science Publishers, 9:113-122, 2008.

Pisalyaput, K. and Tenner, A.J., Complement component C1q inhibits ß-amyloid and serum amyloid P induced neurotoxicity via caspase and calpain-independent mechanisms. J. Neurochem. 104:696-707, 2008.

Lillis, A.P., Greenlee, M.C., Mikhailenko, I., Pizzo, S.V., Tenner, A.J., Strickland, D.K.and Bohlson, S.S. The low-density lipoprotein receptor-related protein (LRP/CD91) is not required for the C1q-triggered enhancement of phagocytosis in murine macrophages. J.Immunol. 181:364-373, 2008.

Tenner, A.J. and Pisalyaput, K., The Complement System in the CNS: Thinking again. In Central Nervous System Diseases and Inflammation, Eds: Thomas E. Lane, Monica Carson, Connie Bergmann, Tony Wyss-Coray, Springer, New York (Invited Review), pp. 153-174, 2008.

Fraser, D.A., Arora, M., Bohlson, S.S., Lozano, E., and Tenner, A.J., Generation of Inhibitory NFkB complexes and pCREB correlates with the anti-inflammatory activity of complement protein C1q in human monocytes. J. Biol. Chem. 282:7360-7367, 2007

Bohlson, S.S., Fraser, D.A., and Tenner, A.J. Complement Proteins C1q and MBL are Pattern Recognition Molecules that Signal Immediate and Long Term Protective Immune Functions. Mol. Immunol. 44:33-43, 2007.

Fraser, D.A., Bohlson, S.S., Jasinskiene, N., Rawal, N., Palmerini, G., Ruiz, S., Rochford, R., and Tenner, A.J., C1q and MBL, components of the innate immune system, influence monocyte cytokine expression, J. Leuk. Biol. 80:107-116, 2006.

Zhou, J., M. I. Fonseca, R. Kayed, S. D. Webster, I. Hernandez, O.Yazan, D. H. Cribbs, C.G. Glabe, and A. J. Tenner, “Novel Aß peptide immunogens modulate plaque pathology and inflammation in a murine model of Alzheimer’s Disease”, J. Neuroinflammation 2:28, 2005.

Bohlson, S.S., Silva, R., Fonseca, M. and Tenner, A.J. CD93 is rapidly shed from the surface of human myeloid cells and the soluble form is detected in human plasma, J. Immunol.175:1239-1247, 2005.

Fan, R. and Tenner, A.J. Differential regulation of Aß42-induced neuronal C1q synthesis and microglial activation. J. Neuroinflammation 2: 1-13, 2005

Bohlson, S.S., Zhang, M., Ortiz, C.E. and Tenner, A.J. The adaptor protein GIPC interacts with CD93 via a class I PDZ binding domain and a highly charged juxtamembrane region of the CD93 cytoplasmic tail. J. Leuk. Biol. 77: 80-89, 2005.

Fonseca, M.I., Zhou, J., Botto, M., and Tenner, A.J. Absence of Complement protein C1q leads to less neuropathology in transgenic mouse models of AD. ,J. Neuroscience 24: 6457-6465, 2004.