NDLI: TCR/CD3 mediated stop-signal is decoupled in T-cells from Ctla4 deficient mice

Content Provider	PubMed Central
Author	Downey, Jos Smith, Andrew Schneider, Helga Hogg, Nancy Rudd, Christopher E.
Copyright Year	2007
Abstract	CTLA-4 is a co-receptor that plays a pivotal role in regulating the threshold for T-cell activation. We recently reported that CTLA-4 ligation can over-ride the stop-signal induced by anti-CD3 ligation [Schneider H, Downey J, Smith A, Zinselmeyer BH, Rush C, Brewer JM, et al. Reversal of the TCR stop-signal by CTLA-4. Science 2006;313:1972]. While these studies compared CTLA-4 positive and negative T-cells from normal mice, little is known regarding the behaviour of T-cells from diseased Ctla4 deficient mice with auto-proliferative disease. In this study, we show that while activated wild-type and Ctla-4−/− T-cells have similar rates of motility, Ctla-4−/− T-cells show a marked resistance to the induction of a stop-signal by anti-CD3 ligation. By contrast, T-cells from normal mice and CD28 deficient mice underwent a normal slowing of motility in response to anti-CD3 ligation. Our findings identify a fundamental difference between normal versus CTLA-4−/− T-cells from diseased mice in the regulation of motility by anti-CD3 ligation. This dysregulation of motility may contribute to the tissue infiltration and the autoimmune disorder observed in Ctla-4−/− mice.
Related Links	http://dx.doi.org/10.1016/j.imlet.2007.09.004
Ending Page	72
Page Count	3
Starting Page	70
File Format	PDF
ISSN	18790542
e-ISSN	18790542
Journal	Immunology letters
Issue Number	1
Volume Number	115
Language	English
Publisher Date	2008-01-15
Access Restriction	Open
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Developmental arrest of NK1.1+ T cell antigen receptor (TCR)- alpha/beta+ T cells and expansion of NK1.1+ TCR-gamma/delta+ T cell development in CD3 zeta-deficient mice

T cells with gamma/delta T cell receptors (TCR) of intestinal type are preferentially expanded in TCR-alpha-deficient lpr mice

Unique CD4+ T cells in TCR α chain-deficient class I MHC-restricted TCR transgenic mice: role in a superantigen-mediated disease process

Immunoglobulin-mediated signal transduction in B cells from CD45- deficient mice

Physical and functional bivalency observed among TCR/CD3 complexes isolated from primary T cells

Altered functional responsiveness of thymocyte subsets from CD3delta-deficient mice to TCR-CD3 engagement.

The interchain disulfide bond between TCR alpha beta heterodimers on human T cells is not required for TCR-CD3 membrane expression and signal transduction.

γδ T Cells from Tolerized αβ T Cell Receptor (TCR)–deficient Mice Inhibit Contact Sensitivity-Effector T Cells In Vivo, and Their Interferon-γ Production In Vitro

CD4-independent signal transduction through the T-cell receptor (TCR/CD3).

TCR/CD3 mediated stop-signal is decoupled in T-cells from Ctla4 deficient mice

Similar Documents

Developmental arrest of NK1.1+ T cell antigen receptor (TCR)- alpha/beta+ T cells and expansion of NK1.1+ TCR-gamma/delta+ T cell development in CD3 zeta-deficient mice

T cells with gamma/delta T cell receptors (TCR) of intestinal type are preferentially expanded in TCR-alpha-deficient lpr mice

Unique CD4+ T cells in TCR α chain-deficient class I MHC-restricted TCR transgenic mice: role in a superantigen-mediated disease process

Immunoglobulin-mediated signal transduction in B cells from CD45- deficient mice

Physical and functional bivalency observed among TCR/CD3 complexes isolated from primary T cells

Altered functional responsiveness of thymocyte subsets from CD3delta-deficient mice to TCR-CD3 engagement.

The interchain disulfide bond between TCR alpha beta heterodimers on human T cells is not required for TCR-CD3 membrane expression and signal transduction.

γδ T Cells from Tolerized αβ T Cell Receptor (TCR)–deficient Mice Inhibit Contact Sensitivity-Effector T Cells In Vivo, and Their Interferon-γ Production In Vitro

CD4-independent signal transduction through the T-cell receptor (TCR/CD3).

TCR/CD3 mediated stop-signal is decoupled in T-cells from Ctla4 deficient mice