PMID- 12960238
OWN - NLM
STAT- MEDLINE
DCOM- 20040109
LR  - 20081121
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 74
IP  - 5
DP  - 2003 Nov
TI  - The role of urokinase-type plasminogen activator (uPA)/uPA receptor in HIV-1 
      infection.
PG  - 750-6
AB  - The binding of urokinase-type plasminogen activator (uPA) to its 
      glycosyl-phosphatidyl-inositol (GPI) anchored receptor (uPAR) mediates a variety 
      of functions in terms of vascular homeostasis, inflammation and tissue repair. 
      Both uPA and uPAR, as well as their soluble forms detectable in plasma and other 
      body fluids, represent markers of cancer development and metastasis, and they 
      have been recently described as predictors of human immunodeficiency virus (HIV) 
      disease progression, independent of CD4+ T cell counts and viremia. A direct link 
      between the uPA/uPAR system and HIV infection was earlier proposed in terms of 
      cleavage of gp120 envelope by uPA. More recently, a negative regulatory effect on 
      both acutely and chronically infected cells has been linked to the noncatalytic 
      portion of uPA, also referred to as the amino-terminal fragment (ATF). ATF has 
      also been described as a major CD8+ T cell soluble HIV suppressor factor. In 
      chronically infected promonocytic U1 cells this inhibitory effect is exerted at 
      the very late stages of the virus life cycle, involving virion budding and 
      entrapment in intracytoplasmic vacuoles, whereas its mechanism of action in 
      acutely infected cells remains to be defined. Since uPAR is a GPI-anchored 
      receptor it requires association with a signaling-transducing component and 
      different partners, which include CD11b/CD18 integrin and a G-protein coupled 
      receptor homologous to that for the bacterial chemotactic peptide 
      formyl-methionyl-leucyl-phenylalanine. Which signaling coreceptor(s) is(are) 
      responsible for uPA-dependent anti-HIV effect remains currently undefined.
FAU - Alfano, Massimo
AU  - Alfano M
AD  - Department of Immunology and Infectious Disease, Vita-Salute University School of 
      Medicine, Milan, Italy.
FAU - Sidenius, Nicolai
AU  - Sidenius N
FAU - Blasi, Francesco
AU  - Blasi F
FAU - Poli, Guido
AU  - Poli G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20030821
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Chemokines)
RN  - 0 (PLAUR protein, human)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Receptors, Urokinase Plasminogen Activator)
RN  - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
SB  - IM
MH  - Chemokines/immunology
MH  - Disease Progression
MH  - HIV Infections/blood/*physiopathology
MH  - HIV-1/*physiology
MH  - Humans
MH  - Receptors, Cell Surface/*physiology
MH  - Receptors, Urokinase Plasminogen Activator
MH  - Urokinase-Type Plasminogen Activator/*physiology
MH  - Virus Replication
RF  - 82
EDAT- 2003/09/10 05:00
MHDA- 2004/01/10 05:00
CRDT- 2003/09/10 05:00
PHST- 2003/09/10 05:00 [pubmed]
PHST- 2004/01/10 05:00 [medline]
PHST- 2003/09/10 05:00 [entrez]
AID - jlb.0403176 [pii]
AID - 10.1189/jlb.0403176 [doi]
PST - ppublish
SO  - J Leukoc Biol. 2003 Nov;74(5):750-6. doi: 10.1189/jlb.0403176. Epub 2003 Aug 21.