Cytotoxic T cells and antibodies

Macrophages, NK cells, and neutrophils

T helper cells and antibodies

T helper cells and cytotoxic T cells

It involves a different epitope from the same pathogen to be presented to B cells

It requires at least 10 days to be fully formed

The response is not as large as that of the primary response

It is associated with somatic hypermutation

T-dependent responses

T-independent responses

Both T-independent and T-dependent responses

Nucleic acids do not stimulate any type of B cell response

Complement must first bind to circulating IgG and then to surface of the pathogen

Complement must bind to two IgG molecules at a minimum

The antibody must first bind complement with its respective Fc receptor

Complement can only be triggered by the IgM antibody isotype

Disassociation (separation) of the five immunoglobulin subunits produces IgG antibody

The partial disassociation of IgM generates secretory IgA

Each immunoglobulin subunit will bind to a different epitope

Each antigen binding site will have the same affinity

Marginal zone B cells

Plasma cells

Memory B cells

Follicular B cells

IgE

IgA

IgM

IgG

The B cell will hold onto the pathogen for phagocytes to identify and phagocytose

The B cell will be killed by the pathogen

The B cell will be able to present pathogen derived antigen to naive T cells for T cell activation

The B cell can become activated

It is an inhibitory ligand for IL-2 on T cells, and binds all available IL-2 which prevents further T cell proliferation

It cleaves the intracellular ITAM motifs from the CD3 and ζ (zeta) chains of T cells, preventing intracellular signal transduction

It replaces the binding of CD28 to B7 (CD80 & CD86), and removes B7 (CD80 & CD86) from the dendritic cell surface

By binding the CTLA-4 receptor on T cells to induce apoptosis in these cells

To induce T cell proliferation

To direct T cell migration to sites of infection

To control T cell proliferation

To increase the affinity of binding in the immune synapse