Memory T cell-mediated resistance to Mycobacterium tuberculosis infection in innately susceptible and resistant mice.
The memory T cell immune response to Mycobacterium tuberculosis infection was examined in strains of mice which vary in their natural susceptibility to Mycobacterium bovis BCG infection. Naturally susceptible (NS) C57BL/6 and naturally resistant (NR) B6D2 F1 hybrid mice were infected with a sublethal dose of M. tuberculosis and then given antibiotic therapy beginning 2 weeks postinfection. T cells from both strains of mice transferred significant levels of resistance to syngeneic mice challenged aerogenically with M. tuberculosis. This memory response was not substantially reduced by depletion of either L3T4+ or Lyt2+ T cells from the donor mice but was ablated by depletion of both T cell subsets. Cyclophosphamide pretreatment of C57BL/6 memory T cell donors also ablated the resistance transferred to recipient mice. In contrast, B6D2 memory T cells were not affected by cyclophosphamide treatment, suggesting that differences may exist in the metabolic state of the memory T cells in the two donor strains, despite the fact that they both develop similar levels of acquired resistance to a subsequent tuberculous challenge.
Hubbard
R D
RD
Trudeau Institute, Inc., Saranac Lake, New York 12983.
Flory
C M
CM
Collins
F M
FM
D000818:Animals; D003520:Cyclophosphamide / Q000494:pharmacology; D007111:Immunity, Cellular; D007116:Immunization, Passive; D007156:Immunologic Memory; D016219:Immunotherapy, Adoptive; D007538:Isoniazid / Q000627:therapeutic use; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009169:Mycobacterium tuberculosis / Q000187:drug effects / Q000254:growth & development / Q000276:immunology*; D012293:Rifampin / Q000627:therapeutic use; D016176:T-Lymphocyte Subsets / Q000276:immunology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D014376:Tuberculosis / Q000188:drug therapy / Q000276:immunology*
D003520:Cyclophosphamide; D007538:Isoniazid; D012293:Rifampin