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Andrea J. Tenner

Researcher at University of California, Irvine

Publications -  167
Citations -  14706

Andrea J. Tenner is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Complement system & Classical complement pathway. The author has an hindex of 64, co-authored 152 publications receiving 13110 citations. Previous affiliations of Andrea J. Tenner include American Red Cross & Oak Ridge National Laboratory.

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Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages

TL;DR: The results suggest that adiponectin is an important negative regulator in hematopoiesis and immune systems and raise the possibility that it may be involved in ending inflammatory responses through its inhibitory functions.
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The role of the anaphylatoxins in health and disease.

TL;DR: Recent findings suggesting that ATs regulate cell apoptosis, lipid metabolism as well as innate and adaptive immune responses through their impact on antigen-presenting cells and T cells are discussed.
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Extensive innate immune gene activation accompanies brain aging, increasing vulnerability to cognitive decline and neurodegeneration: a microarray study

TL;DR: The extent of innate immune gene upregulation in AD was modest relative to the robust response apparent in the aged brain, consistent with the emerging idea of a critical involvement of inflammation in the earliest stages, perhaps even in the preclinical stage, of AD.
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Complement in the Brain

TL;DR: Interestingly, recent animal studies have also indicated that complement activation products are involved in brain development and synapse formation, which may give insights into the role of complement in processes of neurodegeneration and neuroprotection in the injured or aged and diseased adult central nervous system, and thus aid in identifying novel and specific targets for therapeutic intervention.
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Neuronal protection in stroke by an sLex-glycosylated complement inhibitory protein.

TL;DR: A hybrid molecule was used to simultaneously inhibit both complement activation and selectin-mediated adhesion in ischemic neurons and C1q-expressing neurons, inhibited neutrophil and platelet accumulation, and reduced cerebral infarct volumes.