The antibodies bind extracellular virus particles to prevent them from infecting cells

The antibodies bind to extracellular viral particles and target Fc receptor–expressing cytolytic T cell to kill the viruses

 The antibodies bind to viral antigens on the surface of infected cells and promote phagocytosis of the cells

 The antibodies bind to viral antigens on the surface of infected cells and promote complement-mediated lysis of these cells

Opsonisation of antigens for phagocytosis

Mucosal immunity via secretion into the gastrointestinal lumen

Neonatal immunity via placental transfer

Activation of the classical complement pathway

The need for IgE is very rare and so it is only produced in low concentrations

IgE is mainly secreted across the gut lumen and so is not found in the blood

Similar to the alternative complement pathway, IgE spontaneously binds to the surface of molecules and is removed from circulation

The affinity of the IgE Fc receptor is the highest of all the Fc receptors

Complement C1q needs to bind to more than one immunoglobulin molecule to be activated

All antibody isotypes, once bound to their target, have the capacity to activate complement C1q

IgM, with its pentamer structure and 10 antigen binding sites, is the only isotype that can effectively activate the complement system

Once complement C1q is bound to the surface of a pathogen, it can easily activate IgG and IgM

It can activate complement

It will opsonise pathogens in the lumen and force their expulsion

It is a dimer and has 4 antigen binding sites

It has its own Fc receptor on the surface of innate cells

The different T helper subsets will produce different cytokines that act directly on the pathogen

A naïve T cell can potentially become a T helper 1 or T helper 17 cell

The role of T helper cells is to present antigen to B cells to initiate isotype switching

T helper cells are defined by the cytokines they produce following direct contact with pathogen

Cytokines

Integrins

Chemokines

Selectins

Bind to selectins and integrins that line endothelial cells, allowing transmigration of these cells into sites of infection

Facilitate the formation of the immune synapse between them, allowing activation of the T cell

Bind the cytokine IL-1 and promote inflammation

Direct their entry into the lymph node

The proliferation and differentiation of the T cell, generating populations of both T helper and cytotoxic T cells

The generation of a large group of T cells with identical antigen specificity

The expansion of pathogen peptide, to increase the amount of antigen available, to activate sufficient numbers of T cells

The proliferation of T cells, with each T cell expressing a slightly modified TCR, to cover variations in the pathogen-derived antigen

It interacts with any MHC class I molecule presenting viral or tumour peptide

It leaves the lymph node to be reactived by peptide:MHC and CD28

It will present peptide to antigen-specific T cells to secrete cytokines and promote differentiation into the appropriate T helper cell subset

It leaves the lymph node to be reactivated with peptide:MHC