13.3 The Immune System

13.3 The Immune System

Animals meet bacteria, viruses, fungi, and other foreign material constantly. Defense is layered. Innate immunity is already in place and answers quickly. Adaptive immunity is slower the first time, then highly specific, and it remembers.

Innate defenses

Innate immunity does not require a previous infection with that exact microbe. It is fast. It is not antigen-specific in the adaptive sense: the same barriers and cells respond to broad classes of danger rather than to one memorized antigen.

Barriers, phagocytes, and inflammation

Skin is a physical wall. Intact epidermis keeps many microbes outside the body. Mucous membranes line the respiratory and digestive tracts, and mucus traps particles so they can be swept away or swallowed. Secretions add chemical barriers. Stomach acid, enzymes in tears and saliva, and the sticky mucus itself all reduce the chance that a microbe will colonize a surface.

If a pathogen crosses those surfaces, phagocytes such as neutrophils and macrophages engulf and digest it. Engulfing is phagocytosis, and it is something a cell does. An antibody protein cannot wrap itself around a bacterium and swallow it. Phagocytes can, and they are a core innate defense even before any lymphocyte has multiplied.

Inflammation is a local innate response to tissue injury or infection. Chemical signals from damaged cells and from microbes make nearby blood vessels widen and become leakier. Increased blood flow brings warmth and redness. Fluid and phagocytes leave the blood and enter the tissue, which causes swelling. Inflammation brings phagocytes to the damaged site. It is not a memory response to one antigen.

Complement and natural killer cells

Complement is a set of plasma proteins that activate one another in a cascade. Once turned on, complement proteins can puncture some microbial membranes, coat microbes so phagocytes bind them more readily, and attract still more phagocytes to the site. Natural killer cells recognize body cells that look stressed, including many virus-infected cells and some tumor cells, and they kill those cells. They do this without the antigen-specific receptors that T cells use, and they do not secrete antibodies. Barriers, phagocytes, inflammation, complement, and natural killer cells are the innate list to be able to recite.

Adaptive immunity

Adaptive immunity is the work of lymphocytes. It can target a particular molecule, and it changes after the first meeting with that molecule. On a first exposure, only a few lymphocytes bind the new antigen. Those cells must multiply, which takes days. That lag is why the first antibody rise is slow. Later meetings with the same antigen can be much faster because a larger pool of prepared cells already exists.

Antigens and antibodies

An antigen is a molecule the immune system can recognize as foreign or abnormal. A protein on a viral coat and a carbohydrate on a bacterial surface are typical antigens. Receptors usually bind a small region of that molecule rather than the entire particle.

An antibody is a protein, not a cell. B cells that bind the matching antigen can differentiate into plasma cells, and plasma cells secrete large amounts of antibody into blood and other body fluids. This antibody branch is humoral immunity, named for the body fluids where the proteins travel. Each antibody binds a specific antigen. Binding can block a virus from entering a cell, clump particles so they are easier to clear, activate complement, or mark a pathogen so phagocytes eat it. Marking is not eating. The antibody sticks to the antigen. A phagocyte does the engulfing.

Helper T cells and cytotoxic T cells

T lymphocytes handle recognition that depends on antigens displayed on cell surfaces. Helper T cells coordinate. They are activated when they recognize antigen displayed by another cell, and they release signals that stimulate B cells, macrophages, and other T cells. Without that help, many antibody responses stay weak, and other arms of the defense are slower to mobilize. Cytotoxic T cells kill infected cells. They recognize body cells displaying foreign antigen and trigger those cells to die, which stops a virus from using the cell's machinery. Killing infected cells is cell-mediated immunity. Cytotoxic T cells are cells, not antibody proteins, and they are not the cells that pour antibody into the plasma. Plasma cells do that.

MHC proteins, the proteins of the major histocompatibility complex, are the display structures. A cell loads peptide fragments into MHC proteins and places the complexes on its surface. T cells inspect those complexes instead of binding free antigen the way many antibodies do. MHC presentation is how a T cell sees what is inside another cell, or what a phagocyte has digested. MHC proteins are not drugs, and they are not antibodies.

Memory and a second exposure

After an infection clears, or after vaccination, some of the activated lymphocytes remain as memory cells. Vaccination introduces an antigen in a form meant to teach the adaptive system without causing the full disease, so memory can exist before a dangerous exposure. What matters is memory of that antigen, not a product name and not a percent effectiveness.

The same virus, the second time

Picture someone who clears a respiratory virus and meets that same virus again months later. During the first exposure, antibody concentration stays low for several days, then rises and later falls. During the second exposure, memory B cells and memory helper T cells respond promptly. Plasma cells appear sooner, and the antibody concentration rises faster and reaches a higher level than it did the first time. That pattern is the secondary response, and it is specific to the antigen the body has already learned.