Journal
JOURNAL OF IMMUNOLOGY
Volume 191, Issue 3, Pages 1016-1020Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1301236
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Funding
- National Institutes of Health Grants [R01 AI051242, R01 AI084041]
- NATIONAL CANCER INSTITUTE [P30CA016087] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI084041, R01AI051242] Funding Source: NIH RePORTER
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Effector T cells control intracellular infection by secreting cytokines and through contact-dependent cytolysis. Because cytokines can diffuse and act at a distance, we determined whether cytokine diffusion is sufficient to control Mycobacterium tuberculosis or whether direct recognition of infected cells by CD4 T cells is required. Using MHC class II (MHC II) mixed bone marrow chimeras, we compared the bacterial burdens in lung myeloid cells that were capable (MHC II+/+) or not (MHC II-/-) of being recognized by CD4 T cells. MHC II+/+ cells had lower bacterial burdens than did MHC II-/- cells. CD4 T cell depletion increased the number of bacteria associated with MHC II+/+ cells but not MHC II-/- cells, indicating that direct recognition of infected cells by CD4 T cells is required for control of intracellular M. tuberculosis. These results show that the effector mechanisms required for CD4 T cell control of distinct intracellular pathogens differ and that long-range cytokine diffusion does not contribute to control of M. tuberculosis.
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