Human granulocyte-colony stimulation factor (huG-CSF) treatment accelerates anti-dsDNA IgG production in B6.TC mice. Anti-dsDNA IgG production in B6.TC mice (A) and B6 controls (B) that were treated weekly with 1 ug huG-CSF (GCSF) or 5% dextrose (dextrose) starting at 2 months of age (n = 3 per group). Results for B6.TC mice were normalized to their individual anti-dsDNA IgG levels before treatment (week 0) set as 1. Results for B6 were normalized to the average units of all B6.TC mice before treatment to account for the large difference between B6.TC and B6 anti-dsDNA IgG production. (C) Anti-chromatin IgG production in the four cohorts. Unit values are shown because minimal variation was observed before treatment between and within cohorts. The regression lines between the huG-CSF-treated B6.TC and B6 cohorts have significantly different slopes (P = 0.005) but not between dextrose-treated cohorts (P = 0.17). (D) Total serum IgG in the four cohorts. B6.TC mice had significantly more IgG than B6 before treatment (152 vs 95 ug/ml, P = 0.001), but that difference disappeared with time. The huG-CSF treatment did not change total IgG production in neither strain. Anti-dsDNA (E) and chromatin (F) IgG in B6.TC mice normalized to their total IgG production. The autoantibody (autoAb) unit/total IgG ratios were normalized to the individual values before treatment set as 1. The graphs show mean and standard error of the mean at the indicated time points after treatment. For A and E, the P-values correspond to an F-test comparing the slopes for the two linear regression lines corresponding to the two treatments.
Lantow et al. Arthritis Research & Therapy 2013 15:R49 doi:10.1186/ar4208