Our lab investigates cell adhesion mechanisms, and how alterations in adhesion signaling lead to various cardiovascular and inflammatory diseases. In particular, we are interested in studying how blood cells, especially neutrophils adhere to blood vessels and how the dysfunction of their interactions causes inflammation and immune diseases.

Neutrophils are often the first immune cells to reach sites of inflammation, where they release cytotoxic species that kill bacteria, fungi, and other pathogens. Exacerbated inflammation causes collateral tissue damage and is a strong risk factor for cardiovascular diseases such as inflammatory heart disease and stroke. Integrins are transmembrane receptors that control cell adhesion and migration to inflammatory tissues. Such control is particularly important in the vasculature, where dynamic blood flow physically opposes cell attachment. β2 integrins are expressed in all leukocyte populations. We strive to gain a comprehensive understanding of the molecular mechanisms of leukocyte integrin activation in inflammation.

Leukocyte adhesion

Leukocytes circulating in the bloodstream are first captured by the vessel wall, followed by rolling, slow rolling, full activation, and arrest. After arrest, leukocytes further spread and crawl along the vessel until they transmigrate the vessel wall. Rapid neutrophil recruitment is highly dependent on the activation of integrins. We use tools such as flow cytometry, imaging, and genetic intervention to delineate molecules underlying leukocyte adhesion during inflammation.

Molecular mechanisms underlying leukocyte adhesion

Rapid neutrophil recruitment is highly dependent on the activation of integrins. The inside-out integrin activation process receives input from chemokine receptors and relays to intracellualr proteins like kindlin-3. We use total internal reflection fluorescence (TIRF) microscopy in combination with microfluidics to watch integrin activation at the footprints of neutrophils.

Movie: Neutrophil-like HL-60 cell rolling and arrest. CMDR: cell membrane. TagRFP-K3: kindlin-3 labeled with TagRFP, mAb24-AF488: antibody reporter of high-affinity β2 integrin. Flow direction: top to down. 0 s, cell arrest. < 0 s, cell rolling. > 0 s, cell adhesion. Scale bar, 5 µm.

Dynamics of β2 integrin activation in vivo

How are β2 integrins activated during neutrophil adhesion? We generated a β2 integrin activation reporter mice to look at the dynamic β2 integrin activation during leukocyte adhesion in response to inflammatory signals.

Intravital microscopy. 3D reconstruction of β2 integrin activation in mouse neutrophils arresting in response to CXCL1 in vivo. Reporter antibodies show extended integrin (red, top) and high-affinity integrin conformation (green, middle). Channel merge shown in yellow (bottom). Purple, neutrophil cell outlined by Ly6G expression. Scale bar, 5 μm. A, top view. B, side view.

Cellular signaling during inflammatory responses

In response to inflammation, receptor ligation on the membrane of immune cells is transmitted by intracellular second messengers. We aim to understand inter- and intra-cellular signaling using reporter tools including reporter mice for cAMP/cGMP/Ca2+ reporter and β2 integrin activation reporter mice.


Mouse neutrophil integrin activation

in vitro


Mouse neutrophil integrin activation

in vivo

● Biochemistry and molecular biology

● Gene editing and genomic engineering

Multi-color flow cytometry

Transgenic mouse models

Lentiviral and retroviral gene delivery

Bone marrow transplantation


Homogenous antibody binding assays

Molecular structure/function analysis


High-resolution imaging (confocal, super-resolution imaging, live-cell imaging, molecular tracking, TIRF microscopy, FRET microscopy and intravital imaging).