11.1 The Immune System

Phagocytes are white blood cells that provide an early, non-specific immune response by carrying out phagocytosis: they attach to a pathogen, engulf it and digest it.

1. Chemicals from pathogens and attacked body cells attract a phagocyte; movement towards the stimulus is chemotaxis.
2. Receptor proteins on the phagocyte attach to antigens on the pathogen.
3. The cell-surface membrane extends around the pathogen and encloses it in a phagocytic vacuole, or phagosome; this is endocytosis.
4. The phagosome fuses with a lysosome to form a phagolysosome. Lysosomal digestive enzymes enter the vacuole and destroy the pathogen.

Neutrophils are short-lived phagocytes that patrol tissues and are released in large numbers during infection. Macrophages are longer-lived, settle in organs and carry out phagocytosis without completely destroying the pathogen: they display pathogen antigens on their surface as antigen-presenting cells, allowing lymphocytes to recognise them.

Phagocytosis is a non-specific early defence, not antibody production. Neutrophils digest pathogens completely and then die; macrophages have the additional antigen-presentation role that links phagocytosis to later specific immunity. The detailed primary response and memory-cell sequence belong to later cards.

An antigen is a molecular marker on a cell or pathogen surface that allows cell-to-cell recognition. The immune system uses the distinction between self and non-self antigens to decide whether an immune response is stimulated.

• Human body cells carry surface markers that identify them as part of the body.
• Bacteria and viruses carry their own surface markers; antigens can be found on bacterial cell walls or on virus surfaces.
• Some glycolipids and glycoproteins on the outer surface of cell-surface membranes act as antigens.

• Self antigen: produced by the organism’s own body cells; it normally does not stimulate an immune response.
• Non-self antigen: not produced by the organism’s own body cells, including antigens on pathogenic bacteria and viruses; it stimulates an immune response.

An antigen is a recognised surface marker, not necessarily the whole pathogen. Antigen recognition provides the signal for later specific immune responses; the detailed lymphocyte receptor matching, primary-response sequence and memory-cell mechanism belong to the following cards.

A primary immune response is the specific response to a newly encountered non-self antigen. Antigen presentation selects lymphocytes with complementary receptors, which then divide and differentiate into cells that act against the pathogen or infected body cells.

1. A macrophage presents pathogen antigen fragments; antigens may also be displayed on a pathogen or an infected body cell.
2. The B- and T-lymphocytes with receptors complementary to the antigen are selected. This is clonal selection.
3. The selected lymphocytes divide by mitosis, producing many clones with the same antigen specificity. This is clonal expansion.
4. B-cell clones form plasma cells, which secrete antibodies complementary to the antigen. T-cell clones form T-helper cells that stimulate B-cell division and T-killer cells that attach to infected cells and kill them.
5. The antibody response and T-killer action help remove the pathogen or infected cells. The first response is slow because selection, expansion and differentiation take time.

The response is specific because only lymphocytes with complementary receptors are selected. B cells provide the plasma-cell and antibody branch, while T cells provide helper and infected-cell-killing branches. This card stops at the primary effector response; persistent memory and the secondary response are taught separately.

Clonal selection identifies the matching lymphocytes; clonal expansion increases their number. Plasma cells secrete antibodies, whereas T-killer cells kill infected body cells. Do not treat macrophage antigen presentation as antibody production or include memory-cell mechanisms in this primary-response card.

The primary response leaves antigen-specific memory B and T cells in the blood after the infection has been cleared. Their persistence can provide long-term immunity to the same antigen.

• First exposure: the correct lymphocytes are initially scarce, so clonal selection, mitotic expansion and differentiation take time. Plasma cells develop later and begin producing antibodies; symptoms may occur before the response is fully developed.
• Same antigen again: memory cells are already present in larger numbers. They detect the antigen, activate and divide more quickly, producing a faster and stronger secondary response.
• Functional difference: plasma/effector cells act during the immediate response, whereas memory cells persist as a ready population for future exposure. The secondary response produces antibodies more quickly and at a greater concentration, so it may remove the pathogen before symptoms appear.

Primary response → memory B/T cells persist → same antigen is encountered again → matching memory cells activate rapidly → a larger antibody and cellular response removes the pathogen sooner. This memory principle explains how vaccination can provide long-term immunity; vaccine types and vaccination programmes are taught separately.

Memory is specific to the antigen previously encountered, not a general protection against every pathogen. Memory cells are not the same as plasma cells that immediately secrete antibodies, and a faster response does not require invented time, titre or cytokine values.