Document Detail


Involvement of glycoreceptors in galactoxylomannan-induced T cell death.
MedLine Citation:
PMID:  19414751     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The major virulence factor of Cryptococcus neoformans is its capsular polysaccharide, which is also released into tissues. The shed polysaccharide is composed of glucuronoxylomannan, galactoxylomannan (GalXM), and mannoproteins. In a previous study, we demonstrated a direct interaction of purified soluble GalXM with T cells that induced their apoptosis. In this study, we focus on the mechanisms involved in the apoptotic effect of GalXM. In our experimental system, we analyzed the effect of GalXM on purified human T cells and Jurkat cells, a T cell line routinely used for apoptotic studies. Our results reveal that GalXM activates the extrinsic and intrinsic apoptotic pathways through the cleavage and recruitment of caspase-8. Caspase-8 elicits the downstream executioner caspase-3, caspase-6, and caspase-7 both directly and indirectly, via Bid cleavage and caspase-9 activation. These effects appeared to be primarily mediated by the interaction of GalXM with the glycoreceptors, which differed in human T and Jurkat cells. CD45 was primarily involved in Jurkat cells apoptosis while CD7 and CD43 mediated human T cell apoptosis. Our results highlight a new mechanism by which a microbial product can contribute to virulence through direct interaction with T cell glycoreceptors, thereby triggering lymphocyte apoptosis.
Authors:
Eva Pericolini; Elena Gabrielli; Elio Cenci; Magdia De Jesus; Francesco Bistoni; Arturo Casadevall; Anna Vecchiarelli
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  182     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2009 May 
Date Detail:
Created Date:  2009-05-05     Completed Date:  2009-05-26     Revised Date:  2010-09-27    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  6003-10     Citation Subset:  AIM; IM    
Affiliation:
Department of Experimental Medicine and Biochemical Sciences, Microbiology Section, University of Perugia, Perugia, Italy.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Antigens, CD43 / immunology,  metabolism*
Antigens, CD45 / immunology,  metabolism*
Antigens, CD7 / immunology,  metabolism*
Apoptosis / immunology*
Blotting, Western
Caspase 3 / immunology,  metabolism
Caspase 6 / immunology,  metabolism
Caspase 7 / immunology,  metabolism
Cryptococcus neoformans / immunology
Enzyme Activation / immunology
Flow Cytometry
Humans
Immunoblotting
Jurkat Cells
Polysaccharides, Bacterial / immunology*
T-Lymphocytes / immunology,  metabolism*
Grant Support
ID/Acronym/Agency:
AI14209/AI/NIAID NIH HHS; R01 AI033774-16/AI/NIAID NIH HHS; R01AI033774-15/AI/NIAID NIH HHS; R01HL059842-12/HL/NHLBI NIH HHS; R37AI033142/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD43; 0/Antigens, CD7; 0/Polysaccharides, Bacterial; 70903-49-0/galactoxylomannan; EC 3.1.3.48/Antigens, CD45; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 6; EC 3.4.22.-/Caspase 7
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Mesenchymal Stromal Cells Ameliorate Experimental Autoimmune Encephalomyelitis by Inhibiting CD4 Th1...
Next Document:  A network modeling approach to analysis of the th2 memory responses underlying human atopic disease.