This weekend, the American Academy of Allergy, Asthma and Immunology will honor second-year clinical Allergy/Immunology fellow Gitika (Giti) Dhillon, M.D., for her cutting-edge investigations into a rare immune disorder.

Out of a pool of 766 research abstracts accepted and presented at the meeting, the Academy singled out Dhillon's to win the "Interest Section" award for Basic & Clinical Immunology (only seven "Interest Section" awards are presented at the meeting in total). Dhillon will be presented with a plaque, $500 honorarium, and the opportunity to present her findings at a special poster session during the AAAAI's annual meeting, held March 18 to 22 in San Francisco. (Pictured: Dhillon, right, performed the research in collaboration with second-year Allergy/Immunology fellow Carolina Marcus, M.D., left.)

“We’re incredibly proud of Giti and Carolina,” said rheumatologist and associate professor of Medicine Jennifer Anolik, M.D., Ph.D., who directs the lab in which Dhillon and Marcus conducted their research. “Performing research is a requirement for our fellows, as we believe training the next generation of clinician scientists is critical. Even if our fellows don’t pursue their investigations long-term, we want them to be fluent in the rigors of research and able to bring a critical eye to interpreting literature relevant to their field.”

The research zeroed in on Common Variable Immunodeficiency, or CVID – a condition whose name may be a bit of a misnomer. Though one of the most frequent immunodeficiencies (conditions in which the body has trouble manufacturing germ-fighting cells), it’s still relatively rare, affecting only one in 70,000 live births. CVID usually manifests in the teens or twenties, with a person suffering a series of frequent, even repeating respiratory and gastro-intestinal infections – infections that healthy persons would easily fight off once and then develop antibodies to guard against in the future.

To stay healthy and survive, CVID patients need monthly antibody infusions.

“Studying rare conditions – in which bodily processes misfire, or good cells go bad – can actually provide a wealth of information about how our body works when things go right,” Anolik said. “In CVID, we think that there may be a glitch in the process by which immune cells, like B-cells, mature into the swift and powerful germ fighters they are.”

Research into how our bodies churn out and “train” combat-ready B-cells has been a historic strength of URMC immunologists. The vein of study forms the basis of treatments for a whole host of autoimmune diseases, such as multiple sclerosis, lupus and rheumatoid arthritis.

Fellows search for cellular clues

For their study, Dhillon and Marcus worked with Rochester area immunologists to identify a dozen volunteers with CVID, and then age-matched these subjects with healthy “controls,” taking blood samples and observing volunteers in a clinical setting.

The fellows then used state of the art flow cytometry technology (a technique for counting and examining microscopic particles by suspending them in a stream of fluid, and then passing them by an electronic detection device) to analyze B-cells – grouping not only according to various stages in their development (maturation), but by their different functions as “adult” cells. After cataloging cells into distinct populations, she compared each subset of “control” cells (from healthy volunteers) against the corresponding subset from CVID patients.

Any number of factors could be at the root of CVID, Anolik explained, and these side-by-side comparisons might bear clues.

“We wondered if ‘memory’ B-cells may be deficient in some way – particularly in how they are generated in response to infections,” she said.

Or perhaps there was a hiccup in the check-points at which healthy B-cells are screened from bad ones (that is, “auto-reactive” B-cells that mistakenly attack the body's own good tissue), given the association of CVID with autoimmunity. Alternately, Anolik said, CVID might not arise from a problem with the B-cells at all; there could be a communication break-down in the way by which another type of immune cell, helper T-cells, alerts B-cells of imminent danger.

While Dhillon’s and Marcus’s findings are by no means conclusive in pinning down an exact cause of CVID, their research opens an exciting new avenue for understanding how B-cells develop and behave.

Dhillon will present findings and her abstract, “Abnormalities in B Cell Homeostasis and Tolerance in Common Variable Immunodeficiency,” at a special Academy poster session on Sunday, March 20.

“It’s such an honor to win this award and to have worked with Dr. Anolik," Dhillon said.