how do antibodies enable destruction of a pathogen:
recruit complement proteins to enable production of a membrane attack complex, resulting in lysis of the pathogen
enable precipitation of soluble antigens facilitating phagocytosis
opsonise pathogens facilitating phagocytosis
infected cells display processed antigen molecules on their surface via MHC I
CD8 T cell receptors bind to antigen displayed on the surface of infected cells
CD8 T cells release perforins and granzymes which destroy the infected cell
CD8 on the surface of the cytotoxic T lymphocytes bind to MHC I on the surface of the infected cell
CTL stands for
cytotoxic T lymphocyte
the primary immune response is slower than the secondary immune response
the secondary immune response can originate from memory B cells
the primary immune response originates from naive B cells
the secondary response to an antigen lasts longer than the primary immune response
the primary immune response takes over a week to become effective
human influenza virus strains preferentially bind to sialic acids with alpha 2-6 linkage
avian influenza virus strains prefer to bind to sialic acid with alpha 2-3 linkage
helper T cells are vitally important in the acquired immune response because they enable full activation of both the humoral and cell-mediated immune responses
CD8 T cells are activated by antigens presented by an infected or cancerous cell
CD8 T cells bind to an infected cell via:
binding of the T cell receptors with specific antigen presented on the surface of the infected cell
by the interaction of the MHCI on the surface of the infected cell with the CD8 on the cytotoxic T cell
M2 blockers inhibit uncoating of the virus and prevent it from entering the cell