Control of memory CD4 T cell recall by the CD28/B7 costimulatory pathway.

Control of memory CD4 T cell recall by the CD28/B7 costimulatory pathway. Research Abstract Details 

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Control of memory CD4 T cell recall by the CD28/B7 costimulatory pathway. Abstract Text:

Modesta P Ndejembi,John R Teijaro,Deepa S Patke,Adam W Bingaman,Meena R Chandok,Agnes Azimzadeh,Steven G Nadler,Donna L Farber,

The CD28/B7 costimulatory pathway is generally considered dispensable for memory T cell responses, largely based on in vitro studies demonstrating memory T cell activation in the absence of CD28 engagement by B7 ligands. However, the susceptibility of memory CD4 T cells, including central (CD62L(high)) and effector memory (T(EM); CD62L(low)) subsets, to inhibition of CD28-derived costimulation has not been closely examined. In this study, we demonstrate that inhibition of CD28/B7 costimulation with the B7-binding fusion molecule CTLA4Ig has profound and specific effects on secondary responses mediated by memory CD4 T cells generated by priming with Ag or infection with influenza virus. In vitro, CTLA4Ig substantially inhibits IL-2, but not IFN-gamma production from heterogeneous memory CD4 T cells specific for influenza hemagglutinin or OVA in response to peptide challenge. Moreover, IL-2 production from polyclonal influenza-specific memory CD4 T cells in response to virus challenge was completely abrogated by CTLA4Ig with IFN-gamma production partially inhibited. When administered in vivo, CTLA4Ig significantly blocks Ag-driven memory CD4 T cell proliferation and expansion, without affecting early recall and activation. Importantly, CTLA4Ig treatment in vivo induced a striking shift in the phenotype of the responding population from predominantly T(EM) in control-treated mice to predominantly central memory T cells in CTLA4Ig-treated mice, suggesting biased effects of CTLA4Ig on T(EM) responses. Our results identify a novel role for CD28/B7 as a regulator of memory T cell responses, and have important clinical implications for using CTLA4Ig to abrogate the pathologic consequences of T(EM) cells in autoimmunity and chronic disease.

Control of memory CD4 T cell recall by the CD28/B7 costimulatory pathway. Publishing Authors By Initials

MP Ndejembi,JR Teijaro,DS Patke,AW Bingaman,MR Chandok,A Azimzadeh,SG Nadler,DL Farber,

For similar proteins: albumins: ovalbumin research abstracts see: proteins: albumins: ovalbumin research

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Control of memory CD4 T cell recall by the CD28/B7 costimulatory pathway. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 177

Page Numbers: 7698-706

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 1

MONTH: Dec

YEAR: 2006

Control of memory CD4 T cell recall by the CD28/B7 costimulatory pathway. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985117

Control of memory CD4 T cell recall by the CD28/B7 costimulatory pathway. Keywords Mesh Terms:

KEYWORDS: Ovalbumin

MESH TERMS: immunology

Chemical & Substance for Abstract: Control of memory CD4 T cell recall by the CD28/B7 costimulatory pathway. Information

Substance Name: Ovalbumin

Registry Number: 9006-59-1

Grant and Affiliation Information for Control of memory CD4 T cell recall by the CD28/B7 costimulatory pathway.

AFFILIATION: Division of Transplantation, University of Maryland School of Medicine, 685 West Baltimore Street, Baltimore, MD 21201, USA.

Country: United States

AGENCY: United States NIAID

GRANT: AI 50632

ACRONYM: AI

MEDLINETA: J Immunol

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