To determine whether GC formation by activated T cells also occurs in mice, T cells of mice were activated in vitro for 3 days by cross-linking CD3 and CD28.
To further elucidate the role of CD152 in the induction of CCR5, splenocytes of CD152−/− and CD152+/+ mice were activated with anti-CD3 under Th1 polarizing conditions, and upon recall response, analyzed for CCR5 expression on CD4 cells.
Splenocytes and draining lymph node cells from mice immunized with IRBP161-180 on day 13 and control mice were activated with anti-CD3/anti-CD28 antibories or IRBP161-180 to evaluate the production of IFN-γ and IL-17.
To examine if p27 is required for delayed proliferation in Lck-Bcl-2 transgenic mice, purified splenic T cells from Lck-Bcl-2 p27−/− and control mice were activated with immobilized anti-CD3 antibody.
CD4+ T cells isolated from the spleen or peripheral LNs of wild-type BALB/c mice were activated on plate-bound anti-CD3 under Th17 polarizing conditions in the presence or absence of soluble anti-CD28 mAb.
GFP-labeled retinal microglia, isolated from CX3CR1+/GFP mice, were activated with LPS, washed extensively, placed in growth-factor reduced Matrigel, and then injected into the subretinal space of adult wild-type mice.
To determine the role of the NFκB/Rel family of transcription factors in IL-12 plus IL-18-induced IFN-γ transcription, splenic CD4+ T cells from wild type and cRel knockout mice were activated with IL-12 plus IL-18 for 24 hours and the IFN-γ mRNA levels were determined by real-time PCR.
In this study, primary microglia cells harvested from neonatal ICR mice were activated by exposure to hypoxia (1 % O2 for 3 h).
