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Annals of the Rheumatic Diseases logoLink to Annals of the Rheumatic Diseases
. 2002 Nov;61(Suppl 2):ii54–ii58. doi: 10.1136/ard.61.suppl_2.ii54

Protection against tuberculosis: cytokines, T cells, and macrophages

S Kaufmann
PMCID: PMC1766701  PMID: 12379623

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Figure 1 .

Figure 1

Different outcomes of infection with M tuberculosis, different T cell populations involved in protection, and major anti-mycobacterial effector mechanisms of macrophages. This scheme firstly depicts the different outcomes of tuberculosis in healthy and immunocompromised subjects. Secondly, the figure shows the different T cell populations and their major T cell effector mechanisms in the control of disease. Thirdly, the figure shows anti-mycobacterial effector mechanisms of activated macrophages. (Reproduced from Nature Reviews Immunology (vol 1:20–30). Reprinted by permission from Nature Reviews Immunology (2001;1:20–30). Copyright © 2001 Macmillan Magazines Ltd.)

Figure 2 .

Figure 2

Development of granulomatous lesions in tuberculosis. Promptly after infection, T cells and macrophages are attracted to the site of mycobacterial implantation. There, granulomatous lesions develop. As long as the immune response is competent, the lesions will contain bacteria. These productive granulomas represent a focus of highly dynamic interactions between different T cell populations, macrophages of different maturation stages, and dendritic cells. Once immunity weakens, the balance is tipped and the granuloma can no longer contain mycobacteria. Rather, the granulomatous lesion liquefies and bacteria are released to different tissue sites, different organs, and to the environment. Active disease develops and the patient becomes contagious. (For further details see ref 8.)

Figure 3 .

Figure 3

Different antigen presentation pathways in tuberculosis. Mycobacterial antigens reside in the early phagosome. There, their proteins have ready access to MHC class II processing, resulting in potent CD4 T cell stimulation. Phospholigands are produced by these mycobacteria, which stimulate γδ T cells in the absence of known antigen presentation molecules. Presentation of proteins by MHC class I and of glycolipids by CD1 is more complex and probably requires cross priming. Mycobacteria infected macrophages undergo apoptosis. Resulting extracellular vesicles carry antigens to bystander dendritic cells. Uptake of these vesicles results in glycolipid presentation through CD1 and protein presentation through MHC class I. This two cell mechanism can explain stimulation of MHC class I restricted CD8 T cells and of CD1 restricted T cells. (Reproduced from Nature Reviews Immunology (vol 1:20–30). Reprinted by permission from Nature Reviews Immunology (2001;1:20–30). Copyright © 2001 Macmillan Magazines Ltd.)

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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