Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2002 Oct;1(5):279-83.
doi: 10.1016/s1568-9972(02)00065-4.

CD8+ T suppressor cells are back to the game: are they players in autoimmunity?

Affiliations
Review

CD8+ T suppressor cells are back to the game: are they players in autoimmunity?

Gilberto Filaci et al. Autoimmun Rev. 2002 Oct.

Abstract

The CD8+ T suppressor lymphocytes identified in humans belong to three different subpopulations. All of them inhibit the proliferation of antigen-specific T cells. The type 1 and type 2 of CD8+ T suppressor cells are characterized by the CD8+CD28- phenotype, while no detailed data are available at the moment on the phenotype of the type 3 of CD8+ T suppressor cells. The type 1 of CD8+ suppressor T lymphocytes acts by inducing alteration of expression of co-stimulatory molecules on dendritic cells. A cell-to-cell contact is required to mediate this effect. The type 2 of CD8+ T suppressor cells induces inhibition via cytokine secretion (IFNgamma, IL6) and do not need to interact directly with antigen presenting cells. The type 3 of CD8+ T suppressor cells mediates its function through the secretion of IL10. The complexity and multiplicity of CD8+ T suppressor cell subsets suggests that these cells may have an important role in the regulation of the immune homeostasis, acting together with the CD4+ T regulatory cell subpopulations. The specificity of the functions of each of these suppressor/regulatory subsets in the immune network requires to be clarified to better understand the immune system, its functions and the possibilities to modulate its activities in the course of immune-mediated diseases.

PubMed Disclaimer

Similar articles

Cited by

Publication types

LinkOut - more resources