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Mechanisms of strain‐dependent development of mast cells from mouse splenocytes
Author(s) -
Hu ZhiQing,
Zhao WeiHua,
Shimamura Tadakatsu
Publication year - 2006
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/j.1440-1711.2005.01410.x
Subject(s) - splenocyte , spleen , endogeny , mast cell , biology , prostaglandin e , microbiology and biotechnology , cell culture , prostaglandin , cell , immunology , endocrinology , biochemistry , genetics
Mast cell development from spleen cells was not triggered by prostaglandin E 1 (PGE 1 ) or dibutyryl cAMP (db‐cAMP) during a 12 day culture when the spleen cells were obtained from C57BL/6N and DBA/1 mice, but mast cells did develop when the spleen cells were obtained from C3H/HeN, BALB/c and ICR mice. A lack of endogenous IFN‐γ in the initial 2 days of the culture period was responsible for the failure. This was confirmed by adding neutralizing anti‐IFN‐γ antibody and rIFN‐γ to the cultures and by determining IFN‐γ levels in the spleen cell cultures. Th1 cells in the spleens of C57Bl and DBA/1 mice were much more sensitive to PGE 1 and db‐cAMP than Th1 cells from other inbred mice strains, and consequently, IFN‐γ production was inhibited in spleen cell cultures of C57BL and DBA/1 mice on addition of PGE 1 or db‐cAMP. Furthermore, the different sensitivities of Th1 cells to PGE and db‐cAMP were dependent on the different levels of IL‐12 p40 monomers or homodimers in the spleen cell cultures. As the endogenous specific inhibitors of IL‐12 p70 (heterodimers of p40 and p35), large amounts of IL‐12 p40 monomers or homodimers in the spleen cell cultures of C57BL and DBA/1 mice enhanced the ability of PGE 1 and db‐cAMP to inhibit IFN‐γ production by antagonizing the activity of IL‐12 heterodimers. These results indicate that the strain‐dependent development of mast cells from mouse splenocytes is related to endogenous IFN‐γ levels, which are regulated by PGE, db‐cAMP, IL‐12 p70 and IL‐12 p40.