Host surface ectonucleotidase-CD73 and the opportunistic pathogen, Porphyromonas gingivalis, cross-modulation underlies a new homeostatic mechanism for chronic bacterial survival in human epithelial cells

MLA

Jaden S. Lee, et al. “Host Surface Ectonucleotidase-CD73 and the Opportunistic Pathogen, Porphyromonas Gingivalis, Cross-Modulation Underlies a New Homeostatic Mechanism for Chronic Bacterial Survival in Human Epithelial Cells.” Virulence, vol. 11, no. 1, Dec. 2020, pp. 414–29. EBSCOhost, https://doi.org/10.1080/21505594.2020.1763061.

APA

Jaden S. Lee, Nityananda Chowdhury, JoAnn S. Roberts, & Özlem Yilmaz. (2020). Host surface ectonucleotidase-CD73 and the opportunistic pathogen, Porphyromonas gingivalis, cross-modulation underlies a new homeostatic mechanism for chronic bacterial survival in human epithelial cells. Virulence, 11(1), 414–429. https://doi.org/10.1080/21505594.2020.1763061

Chicago

Jaden S. Lee, Nityananda Chowdhury, JoAnn S. Roberts, and Özlem Yilmaz. 2020. “Host Surface Ectonucleotidase-CD73 and the Opportunistic Pathogen, Porphyromonas Gingivalis, Cross-Modulation Underlies a New Homeostatic Mechanism for Chronic Bacterial Survival in Human Epithelial Cells.” Virulence 11 (1): 414–29. doi:10.1080/21505594.2020.1763061.