Differentiation signal defect of splenic cells from LPS-treated mice.
Spleen cells from mice sensitized with 10 microgram of LPS given intravenously are unable, when stimulated in vitro 48 h after this treatment, to respond to sheep erythrocytes (SRBC). Addition of T-cell replacing factors (TRF) to these cells restores their capacity to mount an anti-SRBC immune response. Killing of the cells proliferating under antigen stimulation by highly radioactive thymidine leads to the suppression of the anti-SRBC response observed in the presence of TRF. These experiments suggests that the proliferative events leading to the expansion of B cell precursors under antigen stimulation is not impaired by the treatment by LPS. These preliminary data show that the defect is linked to the lack of signals leading to the differentiation of B cells into antibody-secreting cells.
D000276:Adjuvants, Immunologic / Q000494:pharmacology; D000818:Animals; D000917:Antibody Formation / Q000187:drug effects; D001402:B-Lymphocytes / Q000187:drug effects* / Q000276:immunology; D002454:Cell Differentiation / Q000187:drug effects*; D004926:Escherichia coli; D005260:Female; D007166:Immunosuppressive Agents; D066298:In Vitro Techniques; D015848:Interleukin-5; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008222:Lymphokines; D051379:Mice; D013154:Spleen / Q000166:cytology
D000276:Adjuvants, Immunologic; D007166:Immunosuppressive Agents; D015848:Interleukin-5; D008070:Lipopolysaccharides; D008222:Lymphokines