The Compatibility Gene: How Our Bodies Fight Disease, Attract Others, and Define Our Selves by Daniel M. Davis

Author:Daniel M. Davis [Davis, Daniel M.]
Language: tur
Format: epub
Published: 2014-07-10T23:11:25+00:00

One reason why this is not guaranteed to work out is that there can

be great variety in the tumour cells themselves – even in a single

patient. Even within one person, individual cancer cells can vary in

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The Compatibility Gene

their drug sensitivity. This situation is similar to what we saw with

HIV: a highly variable enemy is more difficult to attack.

Viruses and tumours do something else that’s a problem – they

actively thwart our defences. One way they do this is by trying to

prevent our compatibility genes from working. It’s a battle; our

immune system fights back by checking if compatibility genes have

been interfered with. This involves a whole other function of our

compatibility genes, a different way of looking at the immune system,

and another set of immune genes that are also extremely diverse

among us – in fact, they are probably only second to compatibility

genes in how variable they are from person to person. This next piece

of the canvas – hard-won by new heroes – reveals how compatibility

genes can work in the exact opposite way to what we’ve discussed so far. Breathe it all in, embrace the complexity.

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7

Missing Self

Klas Kärre would later chair the committee that decides the Nobel

Prize in Physiology or Medicine, but in 1981, while writing his PhD

thesis, he was less secure. Trying to summarize his observations in the

last chapter of his thesis, he was puzzled by some data that didn’t

seem consistent with the prevailing ideas about how the immune sys-

tem worked. Kärre – described by his PhD supervisor, Rolf Kiessling,

as soft-spoken, eloquent and slightly absent-minded1 – thought about the problem a lot. Others had come across the same discrepancies but

just didn’t think them particularly important. What often distin-

guishes the great from the everyday scientists is their ability to think

lucidly about observations that don’t fit with contemporary paradigms.

As Leonard Cohen sings, ‘There is a crack in everything, that’s how

the light gets in. ’2

Once again, experiments in transplantation were at the heart of the

matter. Recall that a transplant is rejected whenever it has proteins

detected as non-self which cause an immune attack. But there was an

exception to this rule – first observed in the 1950s by George Snell,

working in the Jackson Laboratory, Maine, USA, a small, independ-

ent non-profit research institution. He discovered a situation in which

transplants would be rejected even when they didn’t have non-self

proteins.

To understand the mystery – to think about it deeply like Kärre

did – we need to consider the genetics of the inbred mice used in

Snell’s experiments. Inbred mice are obtained by successive breeding

between siblings (or parents and their offspring) over long periods. 3

Offspring from two different types of inbred mice are called the

F1 hybrid. Not the cutest of baby names, it stands for Filial 1 hybrid 117

The Compatibility Gene

and is a widely used genetic term to describe offspring from different

strains of animals or plants. For example, a mule is the F1 hybrid of a

male donkey and a female horse. That is, a mule came about when a

donkey and horse mated rather than being a species that evolved

through gradual changes in an ancestor of all three animals.

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