Dark Banquet - Bill Schutt [43]
In far more serious situations, the body’s immune system attacks its own joints (rheumatoid arthritis), transplanted organs, or tissue grafts. To prevent extensive tissue damage or transplant rejection, patients sometimes take immune suppressor drugs. One of the most successful has been ciclosporin (or cyclosporine)—a substance originally isolated from a Norwegian soil fungus. It works by decreasing the activity of T cells (discussed below). Although immune suppressor drugs are often taken for extended periods of time, the dangers of attenuating one’s own immune system should be readily apparent.
Some leukocytes (killer T cells) recognize foreign surface proteins (antigens) and attack any microscopic organisms that “present” them. Other leukocytes (plasma cells, which develop from leukocytes called B cells) produce zillions of tiny bits of protein known as antibodies. Antibodies fit like highly specific keys into locklike receptors on the antigen’s surface. The unfortunate bearer of this gaudy antigen/antibody complex either wobbles off to die or is marked for death in much the same way that a guy with toilet paper stuck to his shoe is marked for ridicule.
Other leukocytes (the oddly named helper T cells) function by helping this immune response to occur, while suppressor T cells throttle down the immune response once the battle is over.
Oh yes, before I forget, some plasma cell precursors called memory T cells stick around the circulatory system once things quiet down. Generally, they’re dormant, but memory T cells are quite capable of jacking up the immune response at a moment’s notice—should the same foolhardy antigen bearer show up again.*62
And one more thing: inoculations for childhood diseases (like mumps) and regional diseases (like yellow fever) work on this principle as well. In many cases, dead or harmless versions of specific pathogens are injected into the body, which manufactures antibodies to combat the perceived threat. Additionally, memory cells stick around to quickly crank up the immune response should the real pathogen ever show up.
Unfortunately, much of what we know about blood was determined only within the past hundred years or so. Sometimes, though, it was a lack of technology, and not blind devotion to old views, that constrained early researchers. Although the concept of humors would not be extinguished completely for nearly four hundred years, soon after the 1628 publication of William Harvey’s landmark book on circulation, Anatomical Studies on the Motion of the Heart and Blood, some physicians began to wonder if the benefits of getting someone else’s blood into a patient’s circulatory system might be greater than draining blood from that person—especially in cases where there had already been significant blood loss.
Dr. Richard Lower performed what is generally considered the first successful blood transfusion in 1666. Using tubing constructed out of goose quills, he connected the carotid artery of one dog (the donor) to the jugular vein of another (the recipient) that he had bled previously to near death. Reportedly, the recipient was resuscitated in a nearly miraculous fashion.
A year later, encouraged by Lower’s results, a Parisian, Jean-Baptiste Denis, used a similar device to infuse about eight ounces of calf blood into the arm of a mentally disturbed man by the name of Antoine Mauroy. Denis, like other researchers of his day, believed that blood carried in it the essence of its owner’s personality. The rationale for the infusion, therefore, was that the “mildness” of the calf’s blood might mellow out Mssr. Mauroy, who police thought was spending a bit too much time running around naked, setting house fires, and beating