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. Author manuscript; available in PMC: 2010 Aug 6.
Published in final edited form as: J Immunol. 2009 Dec 18;184(3):1227–1234. doi: 10.4049/jimmunol.0902011

Fig. 1. Defective phenotypes expressed in CBA/N mice and restoration of BCG performance using adoptive cell transfer approaches.

Fig. 1

Compared to CBA mice, protection against TB challenge after BCG vaccination was significantly (P<0.01, Gohan’s criterion for survival curves) weaker in CBA/N-xid after injection of 5 × 105 M. tuberculosis CFU i. v. (A), or 104 CFU i. t. (B); N = 9 for each group, results presented as mean ± SEM. The defect did not depend upon vaccination dose (C: open bars – non-vaccinated control; black bars −2 × 105 CFU of BCG s. c.; hatched bars −2 × 107 CFU of BCG s. c., challenge − 5 × 105 CFU of M. tuberculosis i. v., N = 8 for each group, mean ± SEM). In CBA → CBA/N radiation bone marrow chimera (9.5 G irradiation, 2 × 107 donor BMC per recipient), protective effect of BCG was restored in terms of both mycobacterial lung CFU counts (D: N = 4 per group, 3 wk post-challenge, P<0.01, one of two similar experiments), and prolongation of survival time (E: N = 8 per group, 2 × 107 CFU of BCG, challenge − 5 × 106 CFU of M. tuberculosis i. v., P<0.05, Gohan’s criterion). Adoptive transfer of 2 × 107/mouse fetal liver (FL) cells from CBA donors to non-irradiated adult CBA/N recipients restored the numbers of B cells in their lymphoid organs to the levels characteristic for the w. t. mice (F) and was sufficient for restoration of BCG-provided protection (G).