Innate immunity

Mast cells release histamine, which makes the endothelial cells of capillaries and venules pull apart so plasma and protein leak out. Fibroblasts and fibrin act later, in repair and walling off.

• Correct: Histamine released by mast cells:
• Collagen laid down by fibroblasts:
• Fibrin formed from fibrinogen:

Neutrophils make up about 50 to 70 percent of leukocytes and arrive at a bacterial infection first. Monocytes follow later and become macrophages.

• Lymphocyte:
• Correct: Neutrophil:
• Monocyte:

The control center compares the incoming value with the set point and sends signals to effectors that move the variable back toward it.

• The effector's output:
• Correct: The set point:
• The afferent pathway:

Innate defenses, such as neutrophils, macrophages and complement, are ready before any exposure and recognize features shared by whole groups of microbes, so they act within minutes to hours of a first encounter.

• Antibodies made specifically against that bacterium: Antibodies against a new antigen take about a week to appear on first exposure, because the lymphocytes that make them must first be selected and multiply.
• Lymphocytes that remember it from before: Lymphocyte memory exists only after a previous exposure. This is the first time.
• Correct: Neutrophils and complement: Correct. Innate defenses are ready at birth and do not need earlier exposure.
• None: every defense needs days to start: Only adaptive immunity takes days on first exposure. The innate layer acts in minutes to hours.

At A the set point has jumped to 39 °C but body temperature is still lower. The hypothalamus treats that gap exactly like cold: sympathetic signals constrict skin vessels, so the skin is pale and cool, and skeletal muscles shiver. The patient feels chilled.

• Correct: Shivering, with pale, cool skin: Correct. Body temperature is below the raised set point, so heat-gain responses run.
• Sweating, with flushed, warm skin: Sweating and flushing are heat-loss responses. They happen at C, when body temperature is above a set point that has dropped.
• Neither, because temperature and set point match: The two lines match at B, not at A. At A the solid line is still below the dashed one.
• Panting to lose heat from the lungs: Panting is a heat-loss response, and at A the body is gaining heat, not losing it.

C5b gathers C6, C7, C8 and C9 into the membrane attack complex. Without C7 the pore cannot form. Neisseria bacteria depend on it most, which is why people lacking C5 to C9 suffer repeated Neisseria infections while coping with most other bacteria.

• Coating bacteria with C3b for phagocytes: C3b is made before C7 is needed, so opsonization still works. That is why she handles most bacteria normally.
• Releasing C3a and C5a to attract neutrophils: C3a and C5a are split off earlier in the cascade, before C7 joins, so inflammation and neutrophil attraction still work.
• Correct: Forming pores that burst the bacteria: Correct. C7 is part of the membrane attack complex, which Neisseria are especially vulnerable to.
• Starting the classical pathway on antibodies: The classical pathway starts with the first complement protein binding antibodies. C7 acts at the end of the cascade, not the start.

The self-identity protein is an NK cell's "leave me alone" signal. A cell that has lost it, especially one also showing stress proteins, tips the balance toward killing. The NK cell releases granules: one protein forms pores, and enzymes enter and trigger apoptosis.

• The NK cell ignores it, because it no longer looks foreign: NK cells work the other way round: they kill cells that lack the normal self signal. Losing it hides a cell from some lymphocytes, but exposes it to NK cells.
• The NK cell engulfs it whole by phagocytosis: NK cells kill by releasing granules onto the target, not by engulfing it.
• The NK cell releases antibodies against the virus: NK cells do not make antibodies. Antibodies come from cells descended from a different line of lymphocytes.
• Correct: The NK cell releases granules that trigger its apoptosis: Correct. Missing the self signal makes the cell a target, and it dies by apoptosis.

When the set point rises, body temperature is below it, not above it. The hypothalamus responds as if you were cold: it constricts skin vessels and starts shivering. Skin vessels dilate only later, when the set point falls again.

• Macrophages that have bound bacteria release pyrogens such as interleukin-1: This step is right. Pyrogens from macrophages start most fevers.
• Pyrogens make cells in the hypothalamus produce prostaglandin E2: This step is right. Prostaglandin E2 is the messenger that resets the hypothalamus.
• The hypothalamic set point rises: This step is right. The set point, not the control system, is what changes.
• Correct: Body temperature is now above the set point, so skin vessels dilate: This is the error. Body temperature is below the raised set point, so skin vessels constrict.
• Heat is conserved and shivering makes more, until temperature reaches the new set point: This step is right. Heat-gain responses raise temperature until it matches the new set point.

Histamine makes the endothelial cells of capillaries and venules pull apart. Plasma proteins leak out, the oncotic difference that holds fluid in the blood shrinks, and fluid filters out faster. Dilated arterioles raise capillary pressure too.

• Neutrophils crowding into the tissue: Neutrophils take hours to arrive, and the number of cells is small compared with the volume of leaked fluid.
• Pus collecting under the skin: Pus forms over a day or more, as neutrophils die. The swelling here appears within minutes.
• Correct: Plasma proteins leaking from venules, so fluid follows: Correct. Leaky vessel walls let protein and fluid pour into the tissue within minutes.
• Complement bursting the cells of the forearm: Your own cells carry regulator proteins that stop the attack complex forming on them.

Cytokines from macrophages at the wound act locally on the vessels and travel in the blood to the bone marrow, the hypothalamus and the liver. The result is a leaky, swollen wound, more circulating neutrophils, a fever and a rise in liver-made inflammatory proteins.

• Permeability of venules at the wound: up. Histamine, prostaglandins, complement fragments and cytokines make the endothelial cells pull apart, so plasma and protein leak into the tissue.
• Neutrophil count in the blood: up. Cytokines reaching the bone marrow make it release stored neutrophils, including young band cells, so the count rises.
• Core body temperature: up. Interleukin-1 and other pyrogens make the hypothalamus produce prostaglandin E2, raising the set point; heat-gain responses then raise body temperature.
• C-reactive protein in the blood: up. Cytokines reaching the liver make it release C-reactive protein and other proteins of inflammation into the blood.

Double-stranded RNA inside a cell is a pattern made when many viruses copy themselves; your own cells do not normally make it in the cytosol. Detecting it switches on type I interferon release, which protects neighboring cells.

• Correct: A virus is copying itself inside; the cell releases interferons: Correct. Viral RNA in the cytosol triggers interferon release.
• A bacterium is on its surface; the cell makes lysozyme: A bacterium on the surface would be detected by surface pattern recognition receptors that bind bacterial wall or flagellum molecules, not by cytosolic sensors for double-stranded RNA.
• The cell is dividing normally; it does nothing: Normal cell division does not put double-stranded RNA in the cytosol, which is why its presence is an alarm signal.
• A worm is nearby; the cell attracts eosinophils: Worms are far too large to get inside a cell, and they are not detected by sensors for viral RNA.