Literature DB >> 8640869

Differential induction of programmed cell death in CD8+ and CD4+ T cells by the B subunit of cholera toxin.

B Yankelevich1, V A Soldatenkov, J Hodgson, A J Polotsky, K Creswell, A Mazumder.   

Abstract

We have recently demonstrated that a short-term treatment of parental splenocytes with the B subunit of cholera toxin (CT-B) abrogates the development of acute GVHD in F1 hybrid mice transplanted with these cells. In order to obtain better insight into the mechanism of the action of CT-B, we studied the effect of CT-B on survival of purified murine T cells and their subsets. We show that treatment with B subunit stimulates apoptosis in T cells, detectable following incubation in vitro. Although apoptosis was noticed in both CD8+ and CD4+ T cell subsets, the treatment preferentially stimulates programmed cell death (PCD) in CD8+ population. Thus, immunosuppressive action of CT-B in vivo may be in part due to its ability to eliminate CD8+ T cells.

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Year:  1996        PMID: 8640869     DOI: 10.1006/cimm.1996.0070

Source DB:  PubMed          Journal:  Cell Immunol        ISSN: 0008-8749            Impact factor:   4.868


  12 in total

1.  Modulation of B-cell proliferative response by a soluble extract of Nippostrongylus brasiliensis.

Authors:  H N Ehigiator; A W Stadnyk; T D Lee
Journal:  Infect Immun       Date:  2000-11       Impact factor: 3.441

2.  Cholera toxin subunit B inhibits IL-12 and IFN-{gamma} production and signaling in experimental colitis and Crohn's disease.

Authors:  E M Coccia; M E Remoli; C Di Giacinto; B Del Zotto; E Giacomini; G Monteleone; M Boirivant
Journal:  Gut       Date:  2005-08-16       Impact factor: 23.059

Review 3.  Direct Manipulation of T Lymphocytes by Proteins of Gastrointestinal Bacterial Pathogens.

Authors:  Robin L Cassady-Cain; Jayne C Hope; Mark P Stevens
Journal:  Infect Immun       Date:  2018-04-23       Impact factor: 3.441

4.  The B subunit of Escherichia coli heat-labile enterotoxin induces both caspase-dependent and -independent cell death pathways in CD8+ T cells.

Authors:  Robert J Salmond; Rachel Williams; Timothy R Hirst; Neil A Williams
Journal:  Infect Immun       Date:  2004-10       Impact factor: 3.441

5.  Differential binding of Escherichia coli enterotoxins LT-IIa and LT-IIb and of cholera toxin elicits differences in apoptosis, proliferation, and activation of lymphoid cells.

Authors:  Sergio Arce; Hesham F Nawar; Michael W Russell; Terry D Connell
Journal:  Infect Immun       Date:  2005-05       Impact factor: 3.441

6.  Escherichia coli heat-labile enterotoxin B subunit is a more potent mucosal adjuvant than its vlosely related homologue, the B subunit of cholera toxin.

Authors:  D G Millar; T R Hirst; D P Snider
Journal:  Infect Immun       Date:  2001-05       Impact factor: 3.441

7.  Escherichia coli enterotoxin B subunit triggers apoptosis of CD8(+) T cells by activating transcription factor c-myc.

Authors:  M Soriani; N A Williams; T R Hirst
Journal:  Infect Immun       Date:  2001-08       Impact factor: 3.441

Review 8.  Cholera toxin: a paradigm of a multifunctional protein.

Authors:  Kaushik Bharati; Nirmal K Ganguly
Journal:  Indian J Med Res       Date:  2011-02       Impact factor: 2.375

9.  Mutant Escherichia coli heat-labile toxin B subunit that separates toxoid-mediated signaling and immunomodulatory action from trafficking and delivery functions.

Authors:  Sylvia A Fraser; Lolke de Haan; Arron R Hearn; Heather K Bone; Robert J Salmond; A Jennifer Rivett; Neil A Williams; Timothy R Hirst
Journal:  Infect Immun       Date:  2003-03       Impact factor: 3.441

10.  Glycosphingolipids as novel targets for T-cell suppression by the B subunit of recombinant heat-labile enterotoxin.

Authors:  R L Truitt; C Hanke; J Radke; R Mueller; J T Barbieri
Journal:  Infect Immun       Date:  1998-04       Impact factor: 3.441

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