Inability of the BCG vaccine to protect mice of the H2 f haplotype at advanced stages of TB infection is associated with defective CD4 + T-cell activation in spleen.

We performed studies in B10.M H2-congenic mouse strain whose H2 ^f haplotype is associated with defective BCG vaccination efficacy against TB challenge. No difference in mortality dynamics between BCG-vaccinated and primarily infected B10.M mice was observed, whereas in B10 (H2 ^b ) congenic mice BCG vaccination significantly prolonged survival. At the early stages of infection, vaccinated mice of both strains controlled mycobacterial multiplication in lungs and draining lymph nodes better than non-vaccinated, however, in B10.M spleens no vaccination effect was evident. More activated cells expressing the CD4 ⁺ CD44 ⁺ CD62L ^- phenotype resided in spleens of vaccinated B10 compared to B10.M mice. Our results suggest that inability of BCG vaccination to prolong survival of TB-infected B10.M mice may be associated with defective response to disseminated rather than primary infection.
Competing Interests: Declaration of competing interest The authors report no conflict of interests.
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