雅思阅读 23: Supercharged Natural Killers（重装上阵的自然杀伤细胞）

改编自 Stanford Medicine / ScienceDaily（2026年8月）。雅思阅读 Section 3 难度，约 1050 词。 素材来源：https://www.sciencedaily.com/releases/2026/08/260824065546.htm

Reading Passage

A. Cell therapies that harness the immune system have transformed the treatment of some cancers of the blood and lymphatic system. Chimeric antigen receptor T cells, engineered in the laboratory to recognise molecular markers on leukaemia cells, now routinely drive otherwise untreatable disease into long remission. Yet solid tumours — which together account for roughly ninety per cent of all human cancer deaths — have stubbornly resisted the same approach. The reason is mechanical and chemical at once. A solid tumour is a dense, fibrous fortress woven from collagen and blood vessels that immune cells struggle to penetrate. Even when a few T cells squeeze through, they encounter a soup of molecular signals deliberately designed to blunt their attack: suppressive cytokines, starving metabolic conditions, and inhibitory proteins on the tumour's own surface. In August 2026, researchers at Stanford Medicine reported a way around the problem in Science Translational Medicine. They have reprogrammed natural killer cells, the immune system's fastest responders, into a specialised tissue-resident form that homes in on tumours, breaks through the barrier and keeps killing once it arrives.

B. Natural killer cells, first identified in the 1970s, are the scouts of the immune system. Unlike B cells and T cells, which must first be introduced to a specific invader before they can respond, natural killer cells recognise and destroy abnormal cells — virally infected or cancerous — within hours, using a balance of activating and inhibitory receptors that distinguishes healthy from diseased tissue. They circulate in the bloodstream, patrolling for trouble. But a subset of these cells does something different: rather than travelling, it settles permanently inside organs such as the skin, lungs, liver and mucosal linings. These so-called tissue-resident cells adopt functions tailored to their local neighbourhood. For decades, immunologists ignored them, focusing on the circulating cells that are easy to sample from a blood draw and easy to grow in a dish. Recent advances in single-cell sequencing and bioinformatics have forced a reappraisal: for many immune responses, the tissue, not the blood, is where the battle is actually won or lost. A circulating cell that never leaves the vessel is a cell that never meets the enemy.

C. The trouble with tissue-resident natural killer cells is that the evidence about them is contradictory. Some studies concluded they are feeble assassins, even helping to suppress immune activity; others found them lethally effective. In the uterine lining, for example, such cells deliberately calm the immune response so that a foetus — half-foreign genetically — is not rejected, and this is a useful trick during pregnancy. But the same cells, summoned to a tumour, would be a fatal liability. The Stanford team reasoned that the tissue-resident population might not be one kind of cell at all, but two lookalike populations with opposite jobs, distinguished not by where they live but by how they were instructed. To test the idea, they took circulating natural killer cells from healthy blood donors and exposed them to cocktails of molecular signals in the laboratory. One signal in particular — transforming growth factor beta, a protein that many cell types, including tumour cells themselves, secrete — proved decisive in driving the cells toward a tissue-resident identity.

D. Dose, it turned out, was everything. A steady, heavy dose of TGF-β over several days produced tissue-resident cells that were dysfunctional and inert, exactly the kind that tumours exploit to protect themselves. A brief, carefully measured pulse of the same molecule, however, produced the opposite: tissue-resident cells bristling with the molecular weaponry of the killer. The recipe also required direct physical contact with epithelial tumour cells; merely placing the two types in the same dish, separated by a permeable membrane, was not enough, suggesting that an additional contact-dependent signal was required. The aggressive cells were distinguishable by a surface marker, CD39, that the passive cells lacked, and they carried heavy loads of perforin — a protein that punches holes in target-cell membranes — alongside granzyme A, a toxic enzyme delivered through those openings. When injected into mice carrying human melanoma or head-and-neck squamous-cell tumours, the engineered cells infiltrated the cancerous tissue and slowed its growth over weeks. Paired with cetuximab, an antibody that flags certain cancer cells for destruction, a single dose kept the animals healthy for thirty days, with no obvious side effects.

E. The practical appeal of the approach extends beyond its biology. Most current immune cell therapies are manufactured individually from a patient's own cells, a process that takes weeks, must pass strict quality checks, and costs hundreds of thousands of pounds per dose. Natural killer cells, by contrast, do not typically trigger dangerous immune reactions when transferred between unrelated people. A single donor, the Stanford group estimates, could supply around twenty treatment doses within a fortnight; the cells can be frozen, stored in a central repository and dispensed like an off-the-shelf drug, with no delay while a bespoke product is manufactured. A Phase I trial in advanced head-and-neck cancer is being prepared, pending regulatory approval. The team cautions, with appropriate restraint, that success in mice is not success in humans, and that the mice in the study were immune-compromised, so the therapy's interaction with a fully functional human immune system remains unproven. Yet the finding marks a shift in immunotherapy's centre of gravity: from engineering T cells in the blood to persuading natural killer cells to take up residence, permanently and aggressively, inside the tumours they are meant to destroy. Whether that shift will survive contact with human biology, as opposed to mouse biology, is the question the coming trial is designed to answer. If it does, the day may come when a cancer patient receives a vial of frozen cells manufactured in a factory rather than a bespoke product grown from their own white blood cells.

Questions 1-4

Choose the correct heading for paragraphs B, C, D and E from the list of headings below.

List of Headings i. Why solid tumours have frustrated cell therapy ii. The discovery that dose determines behaviour iii. Circulating scouts and the cells that stay put iv. How natural killer cells were first discovered in the 1970s v. A contradictory literature and a new hypothesis vi. Why the approach could transform access to treatment vii. The cost of running a Phase I clinical trial

1. Paragraph B: ____
2. Paragraph C: ____
3. Paragraph D: ____
4. Paragraph E: ____

Questions 5-8

Choose the correct letter, A, B, C or D.

5. Why have solid tumours resisted cell therapy? A. They do not produce any molecular signals. B. They are physically hard to enter and chemically suppress immune cells. C. They are too small to be detected by T cells. D. They only occur in the blood.

6. How do tissue-resident natural killer cells differ from circulating ones? A. They travel around the body looking for infection. B. They settle inside organs and adapt to local conditions. C. They are always weaker killers. D. They do not exist in the lungs or liver.

7. What role does TGF-β play in the new method? A. It has no effect on natural killer cells. B. A brief, measured pulse produces aggressive killer cells. C. A heavy, continuous dose produces the best killers. D. It is used only in pregnancy.

8. Why is the new therapy potentially cheaper than existing cell therapies? A. It requires no laboratory equipment. B. It can be produced in batches from one donor and frozen. C. It works without any immune cells. D. It is only used in mice.

Questions 9-13

Do the following statements agree with the claims of the writer?

Write:

• TRUE if the statement agrees with the information
• FALSE if the statement contradicts the information
• NOT GIVEN if there is no information on this

9. Natural killer cells were first identified in the 1970s.
10. Tissue-resident natural killer cells are always weaker killers than circulating ones.
11. The engineered cells worked better when combined with cetuximab.
12. The team tested the new therapy in non-human primates.
13. The Phase I trial has already shown success in human patients.

Questions 14-15

Complete the summary below using NO MORE THAN TWO WORDS from the passage.

The engineered natural killer cells are described as (14) __________ residents, equipped with perforin and (15) __________ to destroy target cells.

答案与解析

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