Our Faculty : Primary Faculty

Daniela Frasca, Ph.D.

Current Research Interest
One major aspect of our current research is the regulation of primary and memory B cell responses to vaccines in healthy individuals of different ages. The age-related impairment in humoral immune responses observed in mice and humans leads to increased frequency and severity of infectious diseases and is responsible for the reduced vaccine responses observed in elderly individuals. The decreased ability of aged individuals to produce high affinity protective antibodies against infectious agents is due to combined defects in B cells, T cells and antigen-presenting cells. Our lab has characterized intrinsic B cell defects occurring in aging mice and humans and has identified several B cell biomarkers that are reduced by aging. These defects include the impairment in the ability of B cells to undergo class switch recombination, which is due to reduced expression of both activation-induced cytidine deaminase (AID) and the E47 transcription factor which transcriptionally activates AID. AID is the enzyme necessary also for somatic hypermutation and is our marker of optimal antibody responses. More recently we have started to identify and characterize functional changes in B cells from obese individuals, either healthy or with Type-2 Diabetes, T2D, and identify molecular mechanisms involved. Obesity represents a significant risk to public health, and obesity-related insulin resistance is considered a major driving force for the development of T2D. Obesity is characterized by chronic low-grade inflammation which has been shown to have a negative impact on immune responses and health outcomes. We have shown that chronic inflammation in obese individuals, similar to what we have observed in the elderly, induces an increase in intrinsic B cell inflammation, which impairs B cell function and antibody production to infectious agents and vaccines.

Research Profile

Pubmed Link