Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

T-cells recognize protein antigens as short peptide fragments (8-20 amino acids) bound to major histocompatibility complex (MHC) molecules on the surface of antigen-presenting cells (APCs). A prerequisite for antigen-specific T-cell activation is antigen uptake, enzymatic degradation, and recycling of MHC-peptide complexes to the surface of APCs. Whereas CD8+ T cells recognize endogenously derived antigen (virus and other intracellular pathogens) bound to MHC class I molecules, CD4+ T cells recognize exogenously derived antigen in complex with MHC class II molecules. Hence, extracellular bacteria, such as meningococci during invasive disease, will be presented to CD4+ T cells in the context of MHC class II molecules, after uptake and processing by professional APCs like B cells, macrophages, or dendritic cells. Antigen-specific CD4+ T cells can be classified as Th1 or Th2 subpopulations on the basis of different cytokine production and effector functions (1). Intracellular microbes often induce Th1-dominated responses, whereas extracellular pathogens and parasites typically trigger Th2 responses. Th1 cells produce mainly interleukin (IL)-2, interferon (IFN)-γ, and tumor necrosis factor (TNF)-β, which represent important inducers of the cell-mediated immune responses. The principal Th1 cytokine IFN-γ activates macrophages by enhancing their ability to phagocytize and destroy microbes by intracellular bactericidal mechanisms. In contrast, Th2 cells produce IL-4, IL-5, IL-6, and IL-13, which are important factors for inducing and regulating B-cell responses (1).

Original publication

DOI

10.1385/1-59259-148-5:339

Type

Journal article

Journal

Methods Mol Med

Publication Date

2001

Volume

66

Pages

339 - 348