title: T-cell responses against meningococcal antigens.
abstract: 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).
authors.affiliation: Department of Vaccinology, National Institute of Public Health, Oslo, Norway.
authors.forename: L M
authors.initials: LM
authors.lastname: Næss
authors.forename: F
authors.initials: F
authors.lastname: Oftung
authors.forename: A
authors.initials: A
authors.lastname: Aase
authors.forename: T E
authors.initials: TE
authors.lastname: Michaelsen
authors.forename: A J
authors.initials: AJ
authors.lastname: Pollard