Table 2.

Summary of the roles of PSGL-1 in bacterial and viral infections.

Type of infection	Example of pathogen	Reported process	Reference
Bacteria	Salmonella typhimurium	PSGL-1/P-selectin interactions lead to neutrophil recruitment and host defenses	(81)
	Staphylococcus aureus	Staphylococcal superantigen-like 5 can bind sLex expressed on PSGL-1 by neutrophils. Therefore, neutrophils cannot be activated or recruited via PSGL-1/P-selectin binding	(82, 83)
	Streptococcus pneumoniae	PSGL-1 is involved in neutrophil phagocytosis through binding to the capsular polysaccharide and cell wall autolysin, LytA	(93)
Viruses	SARS-CoV and SARS-CoV-2	PSGL-1 impairs the incorporation of the viral spike (S) glycoproteins into pseudovirions. Thus, it blocks virus attachment and subsequent infection of target cells	(96)
	Murine leukemia virus	PSGL-1 inactivates murine leukemia virus infectivity	(95)
	Influenza A virus	PSGL-1 disrupts the infectivity of this nonretroviral enveloped virus	(95)
	HIV	In the presence of PSGL-1, the produced HIV particles harbor a defective membrane (without gp120 and gp41). They are therefore ineffective at binding to target cells	(25, 95)
		PSGL-1 cytoplasmic domain (T393) binds F-actin and, therefore, restricts cellular actin dynamics. Without F-actin to recruit, HIV cannot complete the reverse transcription process.	(97)