Reduced up-regulation of memory and adhesion/integrin molecules in susceptible mice and poor expression of immunity to pulmonary tuberculosis.

Previous studies examining the expression of adhesion and integrin molecules on CD4 T lymphocytes generated in response to virulent Mycobacterium tuberculosis infection revealed that certain inbred mouse strains susceptible to breakdown of chronic disease and subsequent reactivation had poor expression of these molecules, which might underlie their inability to adequately focus into lung tissues and mediate protection. The current study examines the possibility that prior vaccination with BCG, or a prior tuberculosis infection, would overcome this deficiency. It was found, however, that this was not the case. Whereas both resistant (C57BL/6) and susceptible (DBA/2, CBA/J) strains were equally well protected in the spleen after intravenous challenge, the latter strains were poorly protected in the lungs regardless of whether the challenge was given by the intravenous or aerosol route. Again, this was associated with poor up-regulation of adhesion and integrin molecules and with histological evidence in memory immune animals of a reduced and delayed influx of T lymphocytes into the lungs.