Abstract:
:Leishmania-induced macrophage (Mphi) dysfunctions have been correlated with altered signaling events. Recent findings from our laboratory suggest that modulation of host protein tyrosine phosphatase (PTP) following Leishmania infection could lead to these Mphi defects. To address this issue, Mphi PTP activity and IFN-gamma-inducible signaling events were evaluated in Leishmania donovani (Ld)-infected cells. We observed that Ld promastigotes can rapidly trigger host PTP activity simultaneously with dephosphorylation of Mphi protein tyrosyl residues and inhibition of protein tyrosine kinase (PTK). Our results further revealed that Mphi SHP-1 PTP was rapidly activated by the infection. This Ld-evoked signaling alteration was reflected by absence of IFN-gamma-induced intracellular phosphorylation. IFN-gamma-inducible JAK2 PTK phosphorylation was also markedly diminished in Ld-infected cells. We also observed that co-immunoprecipitation of JAK2 with SHP-1 was considerably higher in infected as compared to uninfected cells. Altogether, these results suggest that SHP-1-mediated JAK2 dephosphorylation triggered by Leishmania is partly responsible for abnormal Mphi IFN-gamma signaling and represent an important mechanism supporting persistent parasitic infection.
journal_name
Eur J Immunoljournal_title
European journal of immunologyauthors
Blanchette J,Racette N,Faure R,Siminovitch KA,Olivier Mdoi
10.1002/(SICI)1521-4141(199911)29:11<3737::AID-IMMkeywords:
subject
Has Abstractpub_date
1999-11-01 00:00:00pages
3737-44issue
11eissn
0014-2980issn
1521-4141journal_volume
29pub_type
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