@misc{9246475,
  abstract     = {{Cancer immunotherapy targeting the CD40 receptor on antigen presenting cells (APCs) is a promising treatment strategy that promotes priming of tumor-specific T cells and can revert a suppressive tumor microenvironment. CD40 signaling in dendritic cells (DCs) has been shown to promote maturation, enhance expression of MHC, costimulatory molecules and chemokine receptors, and induce IL-12 secretion, resulting in increased priming of CD8+ T cells. Several DC populations have been identified, including conventional DC types 1 and 2 (cDC1s and cDC2s). Yet, how these different DC subsets are affected by CD40 agonistic treatment is still poorly understood. In this project, we investigated CD40 agonistic effects on cDC1s, cDC2s, CD207+ cDC2s, CD11c+ CD14+ cells, and B cells, using a CD40×EpCAM bispecific antibody (bsAb), designed to target both CD40 and the tumor-associated antigen EpCAM. To do so, we established and optimized a method to isolate APCs from tonsillar tissue using FACS and coculture them together with EpCAM-expressing CHO cells while stimulating with the CD40×EpCAM bsAb. The results showed a significant increase in the frequency of CD86+ and CCR7+ B cells after CD40 stimulation. For the DC subsets, no significant upregulation in activation markers could be seen, although the frequency of CD86+ cDC1s showed a positive trend upon stimulation. The method provides a useful in vitro approach for assessing CD40 agonistic effects on APC subsets, but the low number of DCs isolated from tonsillar tissue limits robustness. Additional optimization and experiments with higher cell numbers will be required to draw firm conclusions about differential CD40 activation across DC subsets.}},
  author       = {{Wirehed, Julia and Sert, Beritan}},
  language     = {{eng}},
  note         = {{Student Paper}},
  title        = {{Investigation of CD40 agonistic effects on antigen presenting cell subsets}},
  year         = {{2026}},
}