Dataset Information

The role of ?₂ integrin in dendritic cell migration during infection.

ABSTRACT:

Background

Dendritic cells (DCs) play a key role in shaping T cell responses. To do this, DCs must be able to migrate to the site of the infection and the lymph nodes to prime T cells and initiate the appropriate immune response. Integrins such as ?₂ integrin play a key role in leukocyte adhesion, migration, and cell activation. However, the role of ?₂ integrin in DC migration and function in the context of infection-induced inflammation in the gut is not well understood. This study looked at the role of ?₂ integrin in DC migration and function during infection with the nematode worm Trichuris muris. Itgb2^tm1Bay mice lacking functional ?₂ integrin and WT littermate controls were infected with T. muris and the response to infection and kinetics of the DC response was assessed.

Results

In infection, the lack of functional ?₂ integrin significantly reduced DC migration to the site of infection but not the lymph nodes. The lack of functional ?₂ integrin did not negatively impact T cell activation in response to T. muris infection.

Conclusions

This data suggests that ?₂ integrins are important in DC recruitment to the infection site potentially impacting the initiation of innate immunity but is dispensible for DC migration to lymph nodes and T cell priming in the context of T. muris infection.

SUBMITTER: Altorki T

PROVIDER: S-EPMC7789014 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature

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Publications

The role of β<sub>2</sub> integrin in dendritic cell migration during infection.

Altorki Tarfa T Muller Werner W Brass Andrew A Cruickshank Sheena S

BMC immunology 20210106 1

<h4>Background</h4>Dendritic cells (DCs) play a key role in shaping T cell responses. To do this, DCs must be able to migrate to the site of the infection and the lymph nodes to prime T cells and initiate the appropriate immune response. Integrins such as β<sub>2</sub> integrin play a key role in leukocyte adhesion, migration, and cell activation. However, the role of β<sub>2</sub> integrin in DC migration and function in the context of infection-induced inflammation in the gut is not well under ...[more]

PMID: 33407124

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Project description:BackgroundAdipose-derived stem cells (ASCs) hold a great promise for myocardial infarction, but therapeutic efficacy appears to be limited by their poor survival and engraftment. Integrins are transmembrane proteins known to regulate the biological behaviors of stem cells. Integrin β2 (ITGB2) specifically binds to intercellular cell adhesion molecule-1 (ICAM-1), which is upregulated in infarcted myocardium. ASCs typically express an insufficient amount of ITGB2, and this may limit their homing and engraftment abilities.MethodsASCs were lentivirally transduced to overexpress ITGB2. ITGB2 messenger RNA (mRNA) and protein expression were examined by quantitative polymerase chain reaction (PCR) and western blot. Cell viability, proliferation, and migration were assessed in vitro. Adipogenic and osteogenic differentiation were induced, and the mRNA expressions of specific differentiation markers were quantified by PCR. ICAM-1 expression in the infarcted myocardium was quantified at 3 and 7 days after myocardial infarction. ITGB2-transfected ASCs (ITGB2-ASCs), control ASCs (CTRL-ASCs), and phosphate-buffered saline (PBS) were intramyocardially injected into the peri-infarct region at 3 days after coronary ligation. Four weeks after transplantation, myocardial blood perfusion was measured by 13N·NH3·H2O2 positron emission tomography (PET)/computed tomography (CT). Explanted hearts were then processed for the measurement of capillary density, the quantification of survived green fluorescent protein (GFP+) ASCs, and the identification of ASCs coexpressing angiogenic growth factors.ResultsICAM-1 expression peaked at 3 days after myocardial infarction and remained elevated over the remote normal myocardium at 7 days after myocardial infarction. ITGB2-ASCs displayed a significant increase in cell viability, proliferation rate, and migration index when compared with CTRL-ASCs. Adipogenic and osteogenic differentiation were more enhanced in ITGB2-ASCs than in CTRL-ASCs. Four weeks after transplantation, surviving GFP+ ASCs were significantly increased, ASCs expressing angiogenic growth factors were more pronounced, capillary density was substantially enlarged, and myocardial blood perfusion was markedly improved in the hearts that received ITGB2-ASCs implantation when compared to those that underwent CTRL-ASC treatment.ConclusionsITGB2 overexpression of ASCs enhanced cell viability, proliferation, and migration and induced differentiation in vitro. ITGB2 overexpression significantly improved the survival and engraftment of ASCs into infarcted myocardium via ITGB2/ICAM-1 interaction, augmented angiogenesis, and ultimately improved blood perfusion in infarcted myocardium.

Dataset Information

The role of ?₂ integrin in dendritic cell migration during infection.

Background

Results

Conclusions

Publications

The role of β<sub>2</sub> integrin in dendritic cell migration during infection.

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Dataset Information

The role of ?2 integrin in dendritic cell migration during infection.

Background

Results

Conclusions

Publications

The role of β<sub>2</sub> integrin in dendritic cell migration during infection.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

The role of ?₂ integrin in dendritic cell migration during infection.