Jonathan Uhr dies at 96; researcher shed light on body’s immune system
Jonathan W. Uhr, a medical researcher who expanded the field of immunology with studies that helped explain how antibodies work, led to a therapy that effectively eradicated a blood disorder that could be fatal for newborns, and opened promising new avenues in the treatment of cancer, died Feb. 15 at a hospice center in Dallas. He was 96.
He had prostate cancer, said his wife, Ginger Uhr.
Uhr entered immunology in the 1950s, when relatively little was known about the functioning of the immune system, a complex shield that protects the body from germs and other outside invaders.
Since the late 1700s, doctors had fought smallpox — to cite one example of such an invader — by exposing patients to cowpox, a similar but less virulent virus. That process, an early form of vaccination, was known to provoke an immune response. But precisely how the response worked was unclear until Uhr embarked on his work.
Early in his career, as a researcher at New York University’s medical school, he made several signal discoveries, according to Ellen Vitetta, who collaborated with Uhr for roughly half a century, first at NYU and later at the University of Texas Southwestern medical school in Dallas, where he chaired the department of microbiology.
Uhr’s work centered on antibodies, which are proteins produced by the immune system to fight foreign substances in the body. At the time, Vitetta said, “nobody really knew where they came from or how they were made or what they actually did.”
In studies conducted on guinea pigs, Uhr revealed that immunization with a virus first produced large antibodies, immunoglobulins known as IgM, and then smaller antibodies, immunoglobulins called IgG.
The latter category creates immunological memory, allowing the body to remember a virus or other invader, recognize it and better ward it off in cases of reinfection. Uhr’s findings help explain why vaccination works and why vaccine boosters are sometimes needed.
In further research, he helped make sense of how antibody production is turned on and off. That work was applied most prominently to the study of Rh disease, which stems from an incompatibility in blood types between a pregnant woman and fetus.
If a pregnant woman is Rh negative and the fetus is Rh positive, that fetus and, even more, fetuses in future pregnancies are at risk for developing Rh disease, in which antibodies produced by the mother’s immune system attack the fetus’s red blood cells. In the most severe cases, the disease may result in miscarriage or stillbirth.