Immunology Faculty Member - Beth Stevens, PhD

Beth Stevens, PhD

Boston Children's Hospital
Neurobiology Program - Children's Hospital
CLS 12257, 3 Blackfan Circle
Boston, MA 02115
Tel: 617-919-2979
Fax: 617-219-2772
Visit my lab page here and here.

We are interested in interactions between the two fundamental cell types of the nervous system, neurons and glia. My laboratory seeks to understand how neuron-glia communication facilitates the development and plasticity of synapses—the points of communication between neurons—during both healthy development and disease.

We focus on the role of neural-immune interactions in the patterning of neural circuits. We identified an unexpected role for glia and components of the innate immune system in synaptic pruning. We find that astrocytes induce neuronal expression of complement C1q, the initiating protein of the classical complement cascade. C1q and downstream complement proteins target synapses for elimination by microglia—the resident phagocytes and immune cells of the brain. Our ongoing studies are directed toward defining the cellular and molecular mechanisms underlying microglia-synapse communication in the healthy brain. Using the visual system as our primary model system, we employ a combination of live imaging, molecular, biochemical and neuroanatomical approaches.

Although synapse elimination is largely considered a developmental process, early synapse loss and dysfunction are becoming increasingly recognized as a hallmark of many CNS neurodegenerative diseases. We hypothesize that synapse loss in CNS neurodegenerative diseases, such as Alzheimer’s Disease, is caused by a reactivation, in the mature brain, of similar developmental mechanisms of synapse elimination. In addition, we are investigating the potential link between microglia, immune proteins and synapse loss in the pathogenesis of epilepsy and neurodevelopmental disorders, such as autism.


A microglial cell labeled with green fluorescent protein (GFP). The microglial processes are closely positioned and interacting with retinal ganglion cell inputs (red and turquoise) in the dorsal lateral geniculate nucleus of the thalamus. Image was acquired from a postnatal day 30 mouse.

Last Update: 7/24/2014


For a complete listing of publications click here.



Schafer D, Lehrman E. Kautzman A, Koyama, R, Mardinly A, Greenberg ME, Barres BA, and Stevens, B (2012). Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement dependent Manner Neuron,74; 1-15.

Ji X, Chu Y, Parada I,
Stevens B, Barres BA and Prince C (2010). Enhanced synaptic connectivity and epilepsy in C1q knockout mice. PNAS 107 (17) 7975-80.

Stevens B, Allen NJ, Christopherson KS, Vazquez LE, Nouri N, Howell GR, Micheva KD, Huberman AD, Stafford B, Sher A, Litke, AM, Lambris, JD, Smith SJ, John, SWM, Barres, BA (2007). The classical complement cascade mediates developmental CNS synapse elimination. Cell 131:1164-78.

Ransohoff RM,
Stevens B. 2011. How Many Cell Types Does It Take to Wire a Brain?
Science 333: 1391-92 PMID:21903801

Schafer, DF, Lehrman, E and
Stevens B “Quad-partite” Synapse: Microglia-Synapse Interactions in the Developing and Mature CNS. Glia Jul24 (Special Issue on Microglia) PMID:22829357

Steffan, AH, Barres BA and
Stevens, B (2012) The complement system: an unexpected role in synaptic pruning during development and disease. Annual Reviews Neuroscience 35:369-89 PMID:22715882

Tremblay, ME,
StevensB, SierraA, Wake H, Bessis A, Nummerjahn A (2011) “The role of micoglia in the healthy brain. J Neurosci. 31:16064-9 PMID:22072657

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