Abstract

The tetraspanin, Cluster of Differentiation 151 (CD151), is ubiquitously expressed in adult tissue, especially in the lungs where it has been implicated in lung cancer, asthma, influenza, and idiopathic pulmonary fibrosis (IPF). CD151 interacts with laminin-binding integrins and growth factor receptors, and is reported in cancer-promoting processes such as tumor initiation, metastasis, and angiogenesis. In asthma, CD151 was shown to promote airways hyperresponsiveness through calcium signaling whereas in influenza, CD151 was shown to be a novel host factor for nuclear viral export signaling. Furthermore, CD151 was shown to be associated with increased disease severity and poorer survival outcome in asthma and lung cancer, respectively. In this review, we provide an update on the current understanding of CD151 with regards to its contribution to lung pathophysiology. We also summarize factors that have been shown to regulate CD151 expression and identify key areas that need to be taken into consideration for its utility as a screening or prognostic tool in disease management and/or as a therapeutic target for the treatment of lung diseases.

Highlights

  • Respiratory diseases account for significant illness and premature mortality around the world

  • This study showed that whilst Cluster of Differentiation 151 (CD151) expression was detected on structural or immune cells, these cells secreted CD151-containing exosomes in circulation to act as components for crosstalk between cancer initiating cells and their environment (Yue et al, 2015)

  • Whilst CD151 expression modulation plays a critical role in determining disease progression, whether in promoting pathophysiology of lung cancer, asthma, and influenza or in potentially protecting against idiopathic pulmonary fibrosis (IPF), there is a distinct gap in the literature pertaining to the mechanisms underlying these changes

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Summary

Introduction

Respiratory diseases account for significant illness and premature mortality around the world. The role of CD151 in normal lung physiology is not fully explored but inferences about its critical role can be made from clinical cases of CD151 gene mutation and from studies in mice where CD151 is deleted.

Results
Conclusion

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