IL-2 and IL-3 production in high and low IgG-responding strains of mice

• Published in: Immunology letters Vol. 37; no. 1; p. 91
• Main Authors: Sírová, M, Ríhová, B, Ríha, I, Leipner, C
• Format: Journal Article
• Language: English
• Published: Netherlands 01-07-1993
• Subjects: Animals; Cells, Cultured; Concanavalin A - immunology; Erythrocytes - immunology; Female; Immunoglobulin G - immunology; Interleukin-2 - biosynthesis; Interleukin-3 - biosynthesis; Lymphocyte Activation - immunology; Lymphocytes - immunology; Male; Mice; Mice, Inbred A; Mice, Inbred C57BL; Species Specificity; Spleen - immunology
• ISSN: 0165-2478
• DOI: 10.1016/0165-2478(93)90137-Q

The antibody response of mouse strain C57Bl/10ScSn (B10) is characterized by a low IgG responsiveness to a number of different antigens. Aberrant function of antigen-presenting cells and/or low activity of the Th cell population have been suggested as the cause of the defect. We studied the production of IL-2 and IL-3 in vitro by unstimulated and ConA-stimulated spleen cells. Unstimulated spleen cells of low-responding B10 mice produce significantly less IL-2 compared with the high-responding A/J mice in both intervals tested, i.e. after 24 and 48 h of in vitro incubation. IL-3 production is low but almost comparable in unstimulated cells of both strains. Stimulation of spleen cells by 5 micrograms/ml of ConA leads to considerably higher production of IL-2 in A/J spleen cells. IL-3 production by ConA-stimulated spleen cells showed the same pattern of activity. This low IL-3 production by B10 cells is most likely due to the low production of IL-2 during Th cell activation and to the limited proliferation of these cells. The low IgG production of B10 spleen cells during the secondary response to SRBC in vitro could be restored by IL-2 added to the medium. 50 U/ml of IL-2 increased the number of anti-SRBC IgG-producing cells 40 times in B10 cells, but only 4 times in A/J cells, so that the IgG production in B10 cells reached the same level as that in the A/J cells without exogenous IL-2. We suppose that the limited IL-2 production in the low-responding strain B10 is the cause of the low IgG responsiveness of these mice.