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. Author manuscript; available in PMC: 2019 May 15.
Published in final edited form as: Cancer Res. 2018 Mar 20;78(10):2747–2759. doi: 10.1158/0008-5472.CAN-17-1900

Figure 3. KDM1A pharmacologic inhibition in mice promotes secondary immune response, immunoglobulin class switching and serum paraprotein.

Figure 3

A. Chemical structure of KDM1A inhibitor GSK-LSD1. B. Schedule of administration to mice and immune response elicited by antigen NP-CGG. C. Kdm1a inhibition recapitulates Kdm1a−/− mouse phenotype, with increased monocytes and reduced neutrophils in bone marrow (BM) (left), and causes increased splenic PC in the secondary immune response (right panel). At least n=9 per condition. * p<0.05, *** p<0.001, Mann-Whitney test. Mean and s.e.m. are shown. D. Kdm1a inhibition promotes NP-specific IgG2b antibodies production (high affinity antibodies, which detect the less haptenated antigen NP-4, and total antibodies, which detect the highly haptenated antigen NP-27). At least n=5 per condition. * p<0.05, ** p<0.01, Mann-Whitney test. Mean and s.e.m. are shown. E. Gamma globulin fraction in serum electrophoresis of same mice at day 45. n=10 per condition. * p<0.05, Mann-Whitney test. Mean and s.e.m. are shown.