Thus, splenocytes from both groups of mice were stimulated with macrophage colony-stimulating factor (M-CSF) and RANKL for induction of osteoclastogenesis.
Once stimulation was resumed, mice were stimulated every two days, as before.
Bim mice were stimulated with thioglycollate or LPS and examined for macrophage activation and cytokine production.
ChR2 ILSCm-LP LR) miChR2 ILSCm-LP LRed with the optogenetics US 20 miceafter glutamate receptor antagonist infusion into the LP.
Eight weeks after bone marrow transplantation, the chimeric mice were stimulated with LPS for 6 h, and the livers were isolated to measure the levels of hepcidin mRNA.
Proliferation assays were performed using CD19 or CD81 deficient mice; CFSE-labeled B lymphocytes from wild-type mice and CD19, CD81 and CD38 deficient mice were stimulated with agonistic antibodies against CD38.
To assess if O. ostertagi elicited NET formation in neutrophils from mice, bone marrow neutrophils from C57BL/6 mice were stimulated with OO extract and their ability to release NETs was examined.
Spleen cells from 6.5 TCR-Tg mice were stimulated with 2 μg/ml HA peptide using a Th1 polarizing cytokine cocktail which contained 10 ng/ml hIL12, 10 ng/ml IFNγ and 20 U/ml hIL2.
To investigate the induction of Nur77 expression after TCR cross-linking, thymocytes from Cicf/f and Cicf/fCd4-Cre mice were stimulated with anti-CD3 (5 μg ml−1) and anti-CD28 (10 μg ml−1) for 6 h.
The MRJP3-mediated suppression of IL-4 production was also evident when lymph node cells from OVA/alum-immunized mice were stimulated with OVA plus antigen presenting cells.
BMDMs from WT and Rbpj cKO mice were stimulated with IL-4 (10 ng/mL) for the indicated times.
