Costimulation Blockade in Autoimmunity and Transplantation: The CD28 Pathway | Zendy

Andrew Adams | Zendy; Mandy L. Ford | Zendy; Christian P. Larsen | Zendy

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Costimulation Blockade in Autoimmunity and Transplantation: The CD28 Pathway

Author(s) -

Andrew Adams,

Mandy L. Ford,

Christian P. Larsen

Publication year - 2016

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.1601135

Subject(s) - belatacept , cd80 , abatacept , cd86 , cd28 , immunology , blockade , ctla 4 , autoimmunity , t cell , medicine , transplantation , signal transduction , cancer research , biology , microbiology and biotechnology , immune system , receptor , antibody , kidney transplantation , cytotoxic t cell , cd40 , rituximab , biochemistry , kidney transplant , in vitro

T cell activation is a complex process that requires multiple cell signaling pathways, including a primary recognition signal and additional costimulatory signals. TCR signaling in the absence of costimulatory signals can lead to an abortive attempt at activation and subsequent anergy. One of the best-characterized costimulatory pathways includes the Ig superfamily members CD28 and CTLA-4 and their ligands CD80 and CD86. The development of the fusion protein CTLA-4-Ig as an experimental and subsequent therapeutic tool is one of the major success stories in modern immunology. Abatacept and belatacept are clinically approved agents for the treatment of rheumatoid arthritis and renal transplantation, respectively. Future interventions may include selective CD28 blockade to block the costimulatory potential of CD28 while exploiting the coinhibitory effects of CTLA-4.

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