Donate today to support women in science at Burnet and their work to unlock the vaginal microbiome and reduce risk of HIV infection and preterm birth for women around the world.
Improving the health of vulnerable communities and changing lives is at the heart of what we do and who we are.
Immunoglobulin G (IgG) antibodies that activate Fc-mediated immune functions have been correlated with vaccine efficacy, but it is difficult to unravel the relative roles of multiple IgG and Fc receptor (FcR) features that have the capacity to influence IgG-FcR complex formation but vary on a personalized basis. Here, we develop an ordinary differential-equation model to determine how personalized variability in IgG subclass concentrations and binding affinities influence IgG-FcgammaRIIIa complex formation and validate it with samples from the HIV RV144 vaccine trial. The model identifies individuals who are sensitive, insensitive, or negatively affected by increases in HIV-specific IgG1, which is validated with the addition of HIV-specific IgG1 monoclonal antibodies to vaccine samples. IgG1 affinity to FcgammaRIIIa is also prioritized as the most influential parameter for dictating activation broadly across a population. Overall, this work presents a quantitative tool for evaluating personalized differences underlying FcR activation, which is relevant to ongoing efforts to improve vaccine efficacy.
To create and translate knowledge into better health, so no-one is left behind.
85 Commercial Road, Melbourne
VIC, 3004, Australia
Receive updates and IMPACT magazine.
Copyright © 2023 Burnet Institute. ABN: 49 007 349 984
This website was developed with the generous support of a donor.
Burnet Institute (Australia) is located on the traditional land of the Boon Wurrung people and we offer our respects to their Elders past and present.
We recognise and respect the continuation of cultural, spiritual and educational practices of Aboriginal and Torres Strait Islander peoples of this land.
