Self And The Phenomenon Of Life: A Biologist Examines Life From Molecules To Humanity

(Sean Pound) #1

110 Self and the Phenomenon of Life


b2726 Self and the Phenomenon of Life: A Biologist Examines Life from Molecules to Humanity “9x6”

derived from her own body (autograft) continued to thrive, that from
her brother (allograft) began to degenerate and eventually sloughed off.
Here lies the puzzle, why would the body tolerate a piece of its own skin
but reject one from someone else?^1
Gibson and Medawar, who observed this landmark phenomenon,
reasoned that the host refused to accept the “foreign” skin because it
was “non-self”. For the first time science realized that the human body,
and any animal body for that matter, is endowed with an ability to rec-
ognize self. A transplanted tissue or organ is non-self and therefore has
to be destroyed, just as an invading bacterium should be removed by
the immune system. From then on the concepts of self and immunity
became inseparable in modern medicine. Since immunity is founded on
molecular pattern recognition, there must be a strong molecular basis
for the body to tell self from non-self.
This story reminds us of an earlier example of immunity: blood
transfusion reaction. It was known for some time that if blood is taken
from one species and transfused to another, the red blood corpuscles
from the donor are clumped and broken up, leading to serious illness and
death of the recipient. The same problem frequently happens when blood
is transfused between humans. In 1901, Landsteiner discovered that
human blood can be classified into four groups, called A, B, AB and O.^2
Transfusion within the same group gives no problem, but transfusion
between groups leads to variable outcomes: group A can receive blood
from O, but not from B or AB; group B can receive from O but not A
or AB; group AB can receive from A, B or O; group O cannot receive
blood from any group other than its own type (Table 6.1 and Fig. 6.1).
This complex relationship can be explained in molecular terms. Each
blood type has a unique molecular make-up on the surface of its red
blood cells. The A, B or O types are determined by surface polysaccha-
rides. Each blood group perceives the others as foreign and attempts
to destroy the transfused red cells with host antibodies. No antibodies
are produced against the markers if the host already possesses the same
markers. Thus no reaction takes place when transfusion is within the

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