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It was mind-boggling looking at how immunodeficient these patients were,
because I'd been seeing normal volunteers for three years, and I knew
what someone should do when exposed to this very potent immunogen. We
would immunize the AIDS patients, and they would have no reaction. It
was very fascinating because it was the first time that people were looking
at that. You just don't expect it. Now, it's “Oh sure, of course.” But when it was happening, you were saying, “Wait a minute, I immunized
this guy with five milliliters of KLH; he should have 18,000 units of
antibodies.” But there was nothing. Their T-cells don't respond.
At that time, we didn't have flow cytometry the way we do now. We were
doing laborious physical techniques, like separating the helper cells
from the suppressor cells. We were studying them separately because people
thought there was too much suppression with the imbalance in the helper-suppressor
ratio. We worked on that and looked at these cells. Clearly that wasn't
the case. You could tell. The suppressor cells were there, in fact, they
should have functioned normally, but they couldn't without normal inductive
signals. It was the lack of that inductive signal from the helper cell
that was the defect. So, that was work that we did. That was another New
England Journal of Medicine paper that came out. I think it came out in
1986.
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