Therapeutic blockade of T-cell antigen receptor signal transduction and costimulation in autoimmune disease

Research output: Chapter in Book/Report/Conference proceedingChapter

10 Scopus citations

Abstract

CD4+ T-cell-mediated autoimmune diseases are initiated and maintained by the presentation of self-antigen by antigen-presenting cells (APCs) to self-reactive CD4+ T-cells. According to the two-signal hypothesis, activation of a naïve antigen-specific CD4+ T-cell requires stimulation of both the T-cell antigen receptor (signal 1) and costimulatory molecules such as CD28 (signal 2). To date, the majority of therapies for autoimmune diseases approved by the Food and Drug Administration primarily focus on the global inhibition of immune inflammatory activity. The goal of ongoing research in this field is to develop antigen-specific treatments which block the deleterious effects of self-reactive immune cell function while maintaining the ability of the immune system to clear nonself antigens. To this end, the signaling pathways involved in the induction of CD4+ T-cell anergy, as apposed to activation, are a topic of intense interest. This chapter discusses components of the CD4+ T-cell activation pathway that may serve as therapeutic targets for the treatment of autoimmune disease.

Original languageEnglish (US)
Title of host publicationMultichain Immune Recognition Receptor Signaling
Subtitle of host publicationFrom Spatiotemporal Organization to Human Disease
EditorsAlexander Sigalov
Pages234-251
Number of pages18
DOIs
StatePublished - 2008

Publication series

NameAdvances in Experimental Medicine and Biology
Volume640
ISSN (Print)0065-2598

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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