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Chapter 5 : Delayed-Type Hypersensitivity, Cell-Mediated Immunity, and Antibodies in Tuberculosis

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Abstract:

Both delayed-type hypersensitivity (DTH) and cell-mediated immunity (CMI) are T-lymphocyte responses to bacillary antigens presented mainly by dendritic cells. In tuberculous lesions, DTH kills (nonactivated) macrophages that contain numerous tubercle bacilli when these bacilli release tissue-damaging local concentrations of tuberculin like products. In the resulting (solid) caseous necrosis, bacillary growth is inhibited and many bacilli die because of low oxygen tension and other factors. Therefore, tissue-damaging DTH has apparently evolved in mammals to stop continuing bacillary growth within the nonactivated macrophages that have permitted such growth. In tuberculous lesions, CMI activates macrophages so that they can inhibit and destroy ingested tubercle bacilli. DTH can also activate macrophages if only low local concentrations of tuberculin-like products are present. Both DTH and CMI exert their control locally. Their main systemic manifestation is to provide an expanded antigen-specific lymphocyte population to infiltrate local sites of bacillary lodgement. Antibodies that aid phagocytosis apparently play little or no role in the destruction of the tubercle bacillus. The bacillus readily enters macrophages without being opsonized by antibodies and evidently can multiply intracellularly within nonactivated macrophages in the presence of antibodies. Antigen-antibody reactions at sites of bacillary lodgement result in the production of chemotactic factors, including the C5a component of complement. In immunized hosts, chemotaxins cause a rapid local accumulation of dendritic cells, macrophages, and antigen-specific T cells—all of which would accumulate more slowly without the local antigen-antibody reaction.

Citation: Dannenberg, Jr. A. 2006. Delayed-Type Hypersensitivity, Cell-Mediated Immunity, and Antibodies in Tuberculosis, p 97-119. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch5
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Image of FIGURE 1
FIGURE 1

Cell-mediated immunity producing local activation of macrophages (acquired cellular resistance) in a tuberculous lesion. Dendritic cells, macrophages, and antigen-specific Th1 lymphocytes enter the site from the bloodstream. Dendritic cells (not shown) present the bacillary antigens to the lymphocytes (originally in the draining lymph nodes). The lymphocytes produce lymphokines (LK) (now called cytokines), which activate the macrophages. Only highly activated macrophages are capable of inhibiting or destroying the virulent tubercle bacilli. Reproduced with permission from reference 125.

Citation: Dannenberg, Jr. A. 2006. Delayed-Type Hypersensitivity, Cell-Mediated Immunity, and Antibodies in Tuberculosis, p 97-119. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch5
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Image of FIGURE 2
FIGURE 2

Highly activated macrophages surrounding the caseous center of a 12-day (rabbit) dermal BCG lesion. This figure illustrates an important aspect of effective cell-mediated immunity and acquired cellular resistance, namely, that large numbers of activated (β-galactosidase-positive) macrophages accumulate around a caseous focus, so that bacilli released from dead and dying cells will be ingested by competent rather than incompetent cells. Stained with 5-bromo-4-chloro-3-indolyl-β--galactoside, counterstained with hematoxylin. Magnification, ×90. Reproduced with permission from reference 45.

Citation: Dannenberg, Jr. A. 2006. Delayed-Type Hypersensitivity, Cell-Mediated Immunity, and Antibodies in Tuberculosis, p 97-119. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch5
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Image of FIGURE 3
FIGURE 3

Macrophages in a 21-day rabbit dermal BCG lesion stained both for acid-fast bacilli (red) and for β-galactosidase (to show macrophage activation) (bright blue). (Colors not shown here.) One of these macrophages shows negligible β-galactosidase activity. It contains numerous bacilli and has ruptured. Another macrophage (adjacent) shows high β-galactosidase activity. It contains no bacilli, but is apparently ingesting the bacilli released from the ruptured cell. This figure illustrates how acquired cellular resistance, produced by CMI, stops the local growth of tubercle bacilli, namely, that highly activated macrophages accumulate at the local site and ingest (and destroy) the bacilli released from ineffectual macrophages. Stained with 5-bromo-4-chloro-3-indolyl-β--galactoside, counterstained with hematoxylin, then carbol-fuchsin. Magnification, ×600. Reproduced with permission from reference 29.

Citation: Dannenberg, Jr. A. 2006. Delayed-Type Hypersensitivity, Cell-Mediated Immunity, and Antibodies in Tuberculosis, p 97-119. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch5
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Image of FIGURE 4
FIGURE 4

A group of activated macrophages (epithelioid cells) in a 21-day dermal BCG lesion from a rabbit, stained darkly for the lysosomal enzyme β-galactosidase (bright blue). (Color not shown here.) We use β-galactosidase activity as a histochemical marker for activated macrophages that are capable of destroying tubercle bacilli (29, 40). Although the perifocal tuberculous granulation tissue contains thousands of macrophages, only those macrophages located near tubercle bacilli (and their products) become activated and develop the power to destroy the bacillus. In other words, CMI is mainly a local phenomenon. The darker the macrophage is stained for β-galactosidase, the more it resembles Lurie’s mature epithelioid cell (see glossary), a cell that has destroyed tubercle bacilli (31, 43). Stained with 5-bromo-4-chloro-3-indolyl-β--galactoside, counterstained with hematoxylin. Magnification, ×200. Reproduced with permission from reference 29.

Citation: Dannenberg, Jr. A. 2006. Delayed-Type Hypersensitivity, Cell-Mediated Immunity, and Antibodies in Tuberculosis, p 97-119. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch5
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Image of FIGURE 5
FIGURE 5

(A) Size of primary BCG lesions and reinfection BCG lesions from 3 h to 42 days in rabbits of Experiment I. The reinfected rabbits had been sensitized intradermally by BCG 24 days previously. Note that the reinfection BCG lesions were many times larger than the primary BCG lesions at 3 h, 12 h, and 1, 2, and 3 days (panels A and C), apparently initiated by an antigen-antibody reaction. Note also that the size of the reinfection BCG lesions reached a second peak at 8 days, whereas the primary lesions reached a similar peak at 12 days. These second peaks were apparently caused by an antigen-specific CMI/DTH reaction. After the second peaks, the lesions slowly regressed. Each point represents the mean size of the lesions and its standard error. *P < 0.05; **P < 0.01.

(B) Size of 2-day tuberculin reactions in rabbits of Experiment I. In the reinfected host, tuberculin sensitivity was highest before challenge. This sensitivity declined thereafter, and no booster effect from the second BCG injection was apparent. In contrast, hosts with primary BCG infections developed strong tuberculin sensitivity by 9 days, which tended to remain higher than that present in the reinfected hosts, possibly because the infecting bacilli were not destroyed as readily. Each point represents the mean size of the tuberculin reactions and its standard error.

(C) Size of primary and reinfection BCG lesions and tuberculin reactions in Experiment II, each measured from 3 h to 5 days. As in Experiment I, the reinfected rabbits were sensitized intradermally by BCG 24 days previously.

Note that the reinfection BCG lesions and the tuberculin reactions had a similar pattern, and that the primary BCG lesions remained very small until DTH and CMI started to develop at 4 or 5 days. Each point represents the mean size of the lesions and its standard error. *P < 0.05; **P < 0.01. Reproduced with permission from reference 69.

Citation: Dannenberg, Jr. A. 2006. Delayed-Type Hypersensitivity, Cell-Mediated Immunity, and Antibodies in Tuberculosis, p 97-119. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch5
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Image of FIGURE 6
FIGURE 6

Antibody levels to the mycobacterial 38-kDa secreted antigens (A) PstS-1, (B) HSP65, and (C) PPD in rabbits with primary and reinfection BCG lesions. In the reinfected hosts, the second injection of BCG enhanced all existing antibody levels. In hosts with primary BCG infection, the antibody titer to the secreted 38-kDa antigen PstS-1 became substantial by day 9, but the titers to the constitutive antigens HSP65 and PPD rose more slowly. Each point represents the mean and its standard error.*P < 0.05; **P < 0.01. Reproduced with permission from reference 69.

Citation: Dannenberg, Jr. A. 2006. Delayed-Type Hypersensitivity, Cell-Mediated Immunity, and Antibodies in Tuberculosis, p 97-119. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch5
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References

/content/book/10.1128/9781555815684.ch05
1. Dannenberg, A. M., Jr. 1999. Pathophysiology: basic aspects. I. Pathogenesis of tuberculosis. II. Immunology of tuberculosis, p. 1747. In D. Schlossberg (ed.), Tuberculosis and Nontuberculous Mycobacterial Infections, 4th ed. The W. B. Saunders Co., Philadelphia, Pa.
2. Janeway, C. A., Jr.,, P. Travers,, M. Walport, and, M. J. Shlomchik. 2001. Immunobiology: the Immune System in Health and Disease, 5th ed. Garland Publishing, New York, N.Y.
3. Lewinsohn, D. A.,, A. S. Heinzel,, J. M. Gardner,, L. Zhu,, M. R. Alderson, and, D. M. Lewinsohn. 2003. Mycobacterium tuberculosis-specific CD8+ T cells preferentially recognize heavily infected cells. Am. J. Respir. Crit. Care Med. 168:13461352.
4. Stanford, J. L., and, J. M. Grange. 1974. The meaning and structure of species as applied to mycobacteria. Tubercle 55:143152.
5. Dannenberg, A. M., Jr. 1990. Controlling tuberculosis: the pathologist’s point of view. Res. Micro-biol. 141:192196.
6. McManus, I. C.,, D. N. J. Lockwood,, J. L. Stanford,, M. A. Shaaban,, M. Abdul-Ati, and, G. M. Bahr. 1988. Recognition of a category of responders to group II, slow-grower associated antigens amongst Kuwaiti senior school children, using a statistical model. Tubercle 69:275281.
7. Stanford, J. L. 1997. Newer tuberculins: profile in developing countries, p. 5872. In V. Seth (ed.), Essentials of Tuberculosis in Children. Jaypee Brothers, New Delhi, India.
8. Kaufmann, S. H. E. 2001. How can immunology contribute to the control of tuberculosis? Nat. Rev. Immunol. 1:2030.
9. Daniel, T. M., and, B. W. Janicki. 1978. Mycobacterial antigens: a review of their isolation, chemistry, and immunological properties. Microbiol. Rev. 42:84113.
10. Abou-Zeid, C.,, I. Smith,, J. M. Grange,, T. L. Ratliff,, J. Steele, and, G. A. W. Rook. 1988. The secreted antigens of Mycobacterium tuberculosis and their relationship to those recognized by the available antibodies. J. Gen. Microbiol. 134:531538.
11. Andersen, P.,, D. Askgaard,, L. Ljungqvist,, J. Bennedsen, and, I. Heron. 1991. Proteins released from Mycobacterium tuberculosis during growth. Infect. Immun. 59:19051910.
12. Long, E. R. 1958. The Chemistry and Chemotherapy of Tuberculosis, 3rd ed., p. 106108, 122124. Lippincott Williams & Wilkins, Philadelphia, Pa.
13. Nathan, C., and, R. Yoshida. 1988. Cytokines: interferon-gamma, p. 229251. In J. I. Gallin,, I. M. Goldstein, and, R. Snyderman (ed.), Inflammation: Basic Principles and Clinical Correlates. Raven Press, New York, N.Y.
14. Barnes, P. F.,, S.-J. Fong,, P. J. Brennan,, P. E. Twomey,, A. Mazumder, and, R. L. Modlin. 1990. Local production of tumor necrosis factor and IFN-gamma in tuberculous pleuritis. J. Immunol. 145:149154.
15. Celada, A., and, C. Nathan. 1994. Macrophage activation revisited. Immunol. Today 15:100102.
16. Toossi, Z.,, J. R. Sedor,, J. P. Lapurga,, R. J. Ondash, and, J. J. Ellner. 1990. Expression of functional interleukin 2 receptors by peripheral blood monocytes from patients with active pulmonary tuberculosis. J. Clin. Investig. 85:17771784.
17. Wahl, S. M.,, N. McCartney-Francis,, D. A. Hunt,, P. D. Smith,, L. M. Wahl, and, I. M. Katona. 1987. Monocyte interleukin 2 receptor gene expression and interleukin 2 augmentation of microbicidal activity. J. Immunol. 139:13421347.
18. Holter, W.,, C. K. Goldman,, L. Casabo,, D. L. Nelson,, W. C. Greene, and, T. A. Waldmann. 1987. Expression of functional IL-2 receptors by lipopolysaccharide and interferon-gamma stimulated human monocytes. J. Immunol. 138:29172922.
19. Klebanoff, S. J. 1988. Phagocytic cells: products of oxygen metabolism, p. 391444. In J. I. Gallin,, I. M. Goldstein, and, R. Snyderman (ed.), Inflammation: Basic Principles and Clinical Correlates. Raven Press, New York, N.Y.
20. Beutler, B. 2004. Innate immunity: an overview. Mol. Immunol. 40:845859.
21. Nathan, C., and, M. U. Shiloh. 2000. Reactive oxygen and nitrogen intermediates in the relationship between mammalian hosts and microbial pathogens. Proc. Natl. Acad. Sci. USA 97:88418848.
22. Liew, F. Y., and, F. E. G. Cox. 1991. Nonspecific defence mechanism: the role of nitric oxide. Immunol. Today 12:A17A21.
23. Stuehr, D. J., and, M. A. Marletta. 1987. Induction of nitrite/nitrate synthesis in murine macrophages by BCG infection, lymphokines, or interferon-gamma. J. Immunol. 139:518525.
24. Moncada, S.,, R. M. J. Palmer, and, E. A. Higgs. 1991. Nitric oxide: physiology, patho-physiology, and pharmacology. Pharmacol. Rev. 43:109142.
25. Green, S. J.,, C. A. Nacy, and, M. S. Meltzer. 1991. Cytokine-induced synthesis of nitrogen oxides in macrophages: a protective host response to Leishmania and other intracellular pathogens. J. Leukoc. Biol. 50:93103.
26. Weinberg, J. B. 1998. Nitric oxide production and nitric oxide synthase type 2 expression by human mononuclear phagocytes: a review. Mol. Med. 4:557591.
27. Bogdan, C. 2001. Nitric oxide and the immune response. Nat. Immunol. 2:907916.
28. Chan, J.,, Y. Xing,, R. S. Magliozzo, and, B. R. Bloom. 1992. Killing of virulent Mycobacterium tuberculosis by reactive nitrogen intermediates produced by activated murine macrophages. J. Exp. Med. 175:11111122.
29. Dannenberg, A. M., Jr. 1968. Cellular hyper-sensitivity and cellular immunity in the pathogenesis of tuberculosis: specificity, systemic and local nature, and associated macrophage enzymes. Bacteriol. Rev. 32:85102.
30. Nathan, C., and, M. Sporn. 1991. Cytokines in context. J. Cell Biol. 113:981986.
31. Remick, D. G., and, J. S. Friedland (ed.). 1997. Cytokines in Health and Disease, 2nd ed. Marcel Dekker, Inc., New York, N.Y.
32. Dinarello, C. A.,, M. J. Kluger,, M. C. Powanda, and, J. J. Oppenheim (ed.). 1990. The Physiological and Pathological Effects of Cytokines, p. 81205. Wiley-Liss, New York, N.Y.
33. Rich, A. R. 1951. The Pathogenesis of Tuberculosis, 2nd ed., p. 508569. Charles C Thomas, Springfield, Ill.
34. Lurie, M. B. 1964. Resistance to Tuberculosis: Experimental Studies in Native and Acquired Defensive Mechanisms, p. 77104. Harvard University Press, Cambridge, Mass.
35. Lurie, M. B.,, P. Zappasodi, and, C. Tickner. 1955. On the nature of genetic resistance to tuberculosis in the light of the host-parasite relationships in natively resistant and susceptible rabbits. Am. Rev. Tuberc. 72:297329.
36. Allison, M.,, P. Zappasodi, and, M. B. Lurie. 1962. Host-parasite relationships in natively resistant and susceptible rabbits on quantitative inhalation of tubercle bacilli. Am. Rev. Respir. Dis. 85:553569.
37. Dannenberg, A. M., Jr. 1991. Delayed-type hypersensitivity and cell-mediated immunity in the pathogenesis of tuberculosis. Immunol. Today 12:228233.
38. Dannenberg, A. M., Jr. 1993. Immunopatho-genesis of pulmonary tuberculosis. Hosp. Pract. 28:5158.
39. Dannenberg, A. M., Jr., and, G. A. W. Rook. 1994. Pathogenesis of pulmonary tuberculosis: an interplay of tissue-damaging and macrophage-activating immune responses—dual mechanisms that control bacillary multiplication, p. 459483. In B. R. Bloom (ed.), Tuberculosis: Pathogenesis, Protection, and Control. American Society for Micro-biology, Washington, D.C.
40. Dannenberg, A. M., Jr.,, O. T. Meyer,, J. R. Esterly, and, T. Kambara. 1968. The local nature of immunity in tuberculosis, illustrated histochemically in dermal BCG lesions. J. Immunol. 100:931941.
41. Converse, P. J.,, A. M. Dannenberg, Jr.,, J. E. Estep,, K. Sugisaki,, Y. Abe,, B. H. Schofield,, M. L. M. Pitt. 1996. Cavitary tuberculosis produced in rabbits by aerosolized virulent tubercle bacilli. Infect. Immun. 64:47764787.
42. Sugisaki, K.,, A. M. Dannenberg, Jr.,, Y. Abe,, J. Tsuruta,, W.-J. Su,, W. Said,, L. Feng,, T. Yoshimura,, P. J. Converse, and, P. Mounts. 1998. Nonspecific and immune-specific up-regulation of cytokines in rabbit dermal tuberculous (BCG) lesions. J. Leukoc. Biol. 63:440450.
43. Pearson, B.,, P. L. Wolf, and, J. Vazquez. 1963. A comparative study of a series of new indolyl compounds to localize β-galactosidase in tissues. Lab. Investig. 12:12491259.
44. Yarborough, D. J.,, O. T. Meyer,, A. M. Dannenberg, Jr., and, B. Pearson. 1967. Histo-chemistry of macrophage hydrolases. III. Studies on β-galactosidase, β-glucuronidase and aminopeptidase with indolyl and naphthyl substrates. J. Reticuloendothel. Soc. 4:390408.
45. Shima, K.,, A. M. Dannenberg, Jr.,, M. Ando,, S. Chandrasekhar,, J. A. Seluzicki, and, J. I. Fabrikant. 1972. Macrophage accumulation, division, maturation, and digestive and microbicidal capacities in tuberculous lesions. I. Studies involving their incorporation of tritiated thymidine and their content of lysosomal enzymes and bacilli. Am. J. Pathol. 67:159180.
46. Lurie, M. B. 1932. The correlation between the histological changes and the fate of living tubercle bacilli in the organs of tuberculous rabbits. J. Exp. Med. 55:3152.
47. Dannenberg, A. M., Jr. 1989. Immune mechanisms in the pathogenesis of pulmonary tuberculosis. Rev. Infect. Dis. 11(Suppl. 2):S369S378.
48. Ando, M.,, A. M. Dannenberg, Jr.,, M. Sugimoto, and, B. S. Tepper. 1977. Histochemical studies relating the activation of macrophages to the intracellular destruction of tubercle bacilli. Am. J. Pathol. 86:623634.
49. Lurie, M. B. 1939. Studies on the mechanism of immunity in tuberculosis. The role of extracellular factors and local immunity in fixation and inhibition of growth of tubercle bacilli. J. Exp. Med. 69:555578.
50. Matzinger, P. 2002. The danger model: a renewed sense of self. Science 296:301305.
51. Matzinger, P. 1994. Tolerance, danger, and the extended family. Annu. Rev. Immunol. 12:9911045.
52. Gallucci, S., and, P. Matzinger. 2001. Danger signals: SOS to the immune system. Curr. Opin. Immunol. 13:114119.
53. Chen, L. 2004. Co-inhibitory molecules of the B7-CD28 family in the control of T-cell immunity. Nat. Rev. Immunol. 4:336347.
54. Suga, M.,, A. M. Dannenberg, Jr., and, S. Higuchi. 1980. Macrophage functional heterogeneity in vivo: macrolocal and microlocal macrophage activation, identified by double-staining tissue sections of BCG granulomas for pairs of enzymes. Am. J. Pathol. 99:305324.
55. Nathan, C. F. 1987. Secretory products of macrophages. J. Clin. Investig. 79:319326.
56. Grage-Griebenow, E.,, H.-D. Flad, and, M. Ernst. 2001. Heterogeneity of human peripheral blood monocyte subsets. J. Leukoc. Biol. 69:1120.
57. Ragno, S.,, M. Romano,, S. Howell,, D. J. C. Pappin,, P. J. Jenner, and, M. J. Colston. 2001. Changes in gene expression in macrophages infected with Mycobacterium tuberculosis: a combined transcriptomic and proteomic approach. Immunology 104:99108.
58. Ando, M.,, A. M. Dannenberg, Jr.,, M. Sugimoto, and, B. S. Tepper. 1977. Histochemical studies relating the activation of macrophages to the intracellular destruction of tubercle bacilli. Am. J. Pathol. 86:623634.
59. Lurie, M. B.,, P. Zappasodi,, E. Cardona-Lynch, and, A. M. Dannenberg, Jr. 1952. The response to the intracutaneous inoculation of BCG as an index of native resistance to tuberculosis. J. Immunol. 68:369387.
60. Lurie, M. B., and, A. M. Dannenberg, Jr. 1965. Macrophage function in infectious disease with inbred rabbits. Bacteriol. Rev. 29:466476.
61. Ellner, J. J. 1997. Regulation of the human immune response during tuberculosis. J. Lab. Clin. Med. 130:469475.
62. Ellner, J. J. 1996. Immunosuppression in tuberculosis. Infect. Agents Dis. 5:6272.
63. Ellner, J. J. 1997. Review: the immune response in human tuberculosis—implications for tuberculosis control. J. Infect. Dis. 176:13511359.
64. Thompson, N. J.,, J. L. Glassroth,, D. E. Snider, Jr., and, L. S. Farer. 1979. The booster phenomenon in serial tuberculin testing. Am. Rev. Respir. Dis. 119:587597.
65. Menzies, D. 1999. Interpretation of repeated tuberculin tests. Boosting, conversion, and reversion. Am. J. Respir. Crit. Care Med. 159:1521.
66. Comstock, G. W., and, S. F. Woolpert. 1978. Tuberculin conversion: true or false? Am. Rev. Respir. Dis. 118:215217. (Editorial.)
67. Demissie, A.,, P. Ravn,, J. Olobo,, T. M. Doherty,, T. Eguale,, M. Geletu,, W. Hailu,, P. Andersen, and, S. Britton. 1999. T-cell recognition of Mycobacterium tuberculosis culture filtrate fractions in tuberculosis patients and their household contacts. Infect. Immun. 67:59675971.
68. Ravn, P.,, A. Demissie,, T. Eguale,, H. Wondwosson,, D. Lein,, H. A. Amoudy,, A. S. Mustafa,, A. K. Jensen,, A. Holm,, I. Rosenkrands,, F. Oftung,, J. Olobo,, F. von Reyn, and, P. Andersen. 1999. Human T cell responses to the ESAT-6 antigen from Mycobacterium tuberculosis. J. Infect. Dis. 179:637645.
69. Doherty, T. M.,, A. Demissie,, J. Olobo,, D. Wolday,, S. Britton,, T. Eguale,, P. Ravn, and, P. Andersen. 2002. Immune responses to the Mycobacterium tuberculosis-specific antigen ESAT-6 signal subclinical infection among contacts of tuberculosis patients. J. Clin. Microbiol. 40:704706.
70. Shigenaga, T.,, A. M. Dannenberg, Jr.,, D. B. Lowrie,, W. Said,, M. J. Urist,, H. Abbey,, B. H. Schofield,, P. Mounts, and, K. Sugisaki. 2001. Immune responses in tuberculosis: antibodies and CD4-CD8 lymphocytes with vascular adhesion molecules and cytokines (chemokines) cause a rapid antigen-specific cell infiltration at sites of bacillus Calmette-Guérin reinfection. Immunology 102:466479.
71. Laal, S.,, K. M. Samanich,, M. G. Sonnenberg,, S. Zolla-Pazner,, J. M. Phadtare, and, J. T. Belisle. 1997. Human humoral responses to antigens of Mycobacterium tuberculosis: immunodominance of high-molecular-mass antigens. Clin. Diagn. Lab. Immunol. 4:4956.
72. Samanich, K. M.,, J. T. Belisle,, M. G. Sonnenberg,, M. A. Keen,, S. Zolla-Pazner, and, S. Laal. 1998. Delineation of human antibody responses to culture filtrate antigens of Mycobacterium tuberculosis. J. Infect. Dis. 178:15341538.
73. Barksdale, L., and, K.-S. Kim. 1977. Mycobacterium. Bacteriol. Rev. 41:217372.
74. Cardona, P. J.,, E. Julián,, X. Vallès,, S. Goradillo,, M. Munõs,, M. Luquin, and, V. Ausina. 2002. Production of antibodies against glycolipids from the Mycobacterium tuberculosis cell wall in aerosol murine models of tuberculosis. Scand. J. Immunol. 55:639645.
75. Guirado, E.,, I. Amat,, O. Gil,, J. Diaz,, V. Arcos,, N. Caceres,, V. Ausina, and, P. J. Cardona. 2006. Passive-serum therapy with polyclonal antibodies against Mycobacterium tuberculosis protects against post-chemotherapy relapse of tuberculosis infection in SCID mice. Microbes Infect. [E-pub ahead of print.]
76. Glatman-Freedman, A., and, A. Casadevall. 1998. Serum therapy for tuberculosis revisited: reappraisal of the role of antibody-mediated immunity against Mycobacterium tuberculosis. Clin. Microbiol. Rev. 11:514532.
77. Glatman-Freedman, A. 2003. Advances in antibody-mediated immunity against Mycobacterium tuberculosis: implications for a novel vaccine strategy. FEMS Immunol. Med. Microbiol. 39:916.
78. Rich, A. R. 1951. The Pathogenesis of Tuberculosis, 2nd ed., p. 570613. Charles C Thomas Publishers, Springfield, Ill.
79. Laal, S., and, Y. A. W. Skeiky. 2005. Immune-based methods, p. 7183. In S. T. Cole,, K. D. Eisenach,, D. N. McMurray, and, W. R. Jacobs, Jr. (ed.), Tuberculosis and the Tubercle Bacillus. ASM Press, Washington, D.C.
80. Reggiardo, Z., and, G. Middlebrook. 1974. Failure of passive serum transfer of immunity against aerogenic tuberculosis in rabbits. Proc. Soc. Exp. Biol. Med. 145:173175.
81. Sethna, K. B.,, N. F. Mistry,, Y. Dholakia,, N. H. Antia, and, M. Harboe. 1998. Longitudinal trends in serum levels of mycobacterial secretory (30 kD) and cytoplasmic (65 kD) antigens during chemo-therapy of pulmonary tuberculosis patients. Scand. J. Infect. Dis. 30:363369.
82. Wiker, H. G.,, S. L. Michell,, R. G. Hewinson,, E. Spierings,, S. Nagai, and, M. Harboe. 1999. Cloning, expression and significance of MPT53 for identification of secreted proteins of Mycobacterium tuberculosis. Microb. Pathog. 26:207219.
83. Majno, G., and, I. Joris. 1996. Cells, Tissues, and Disease: Principles of General Pathology, p. 530532. Blackwell Science, Cambridge, Mass.
84. Cooper, N. R. 1999. Biology of the complement system, p. 281315. In J. I. Gallin,, R. Snyderman,, D. T. Fearon,, B. F. Haynes, and, C. Nathan (ed.), Inflammation:Basic Principles and Clinical Correlates, 3rd ed. Lippincott Williams & Wilkins, Philadelphia, Pa.
85. Regnault, A.,, D. Lankar,, V. Lacabanne,, A. Rodriguez,, C. Thery,, M. Rescigno,, T. Saito,, S. Verbeek,, C. Bonnerot,, P. Ricciardi-Castagnoli, and, S. Amigorena. 1999. Fc gamma receptor-mediated induction of dendritic cell maturation and major histocompatibility complex class 1-restricted antigen presentation after immune complex internalization. J. Exp. Med. 189:371380.
86. Rumsaeng, V.,, W. W. Cruikshank,, B. Foster,, C. Prussin,, A. S. Kirshenbaum,, T. A. Davis,, H. Kornfeld,, D. M. Center, and, D. D. Metcalfe. 1997. Human mast cells produce the CD4+T lymphocyte chemoattractant factor, IL-16. J. Immunol. 59:29042910.
87. Crooks, S. W., and, R. A. Stockley. 1998. Leukotriene B4. Int. J. Biochem. Cell Biol. 30:173178.
88. Lam, B. K., and, K. F. Austen. 1992. Leukotrienes: biosynthesis, release, and actions, p. 13947. In J. I. Gallin,, I. M. Goldstein, and, R. Snyderman (ed.), Inflammation: Basic Principles and Clinical Correlates, 2nd ed. Raven Press, Ltd, New York, N.Y.
89. Yuan, D.,, C. Y. Koh, and, J. A. Wilder. 1994. Interactions between B lymphocytes and NK cells. FASEB J. 8:10121018.
90. Smith, R. S.,, T. J. Smith,, T. M. Blieden, and, R. P. Phipps. 1997. Fibroblasts as sentinel cells. Synthesis of chemokines and regulation of inflammation. Am. J. Pathol. 151:317322.
91. Gosset, P.,, I. Tillie-Leblond,, S. Oudin,, O. Parmentier,, B. Wallaert,, M. Joseph, and, A.-B. Tonnel. 1999. Production of chemokines and proinflammatory and antiinflammatory cytokines by human alveolar macrophages activated by IgE receptors. J. Allergy Clin. Immunol. 103:289297.
92. Ying, S.,, L. T. Barata,, Q. Meng,, J. A. Grant,, J. Barkans,, S. R. Durham, and, A. B. Kay. 1998. High-affinity immunoglobulin E receptor (Fc (RI)-bearing eosinophils, mast cells, macrophages and Langerhans’ cells in allergen-induced late-phase cutaneous reactions in atopic subjects. Immunology 93:281288.
93. Nilsson, G.,, J. J. Costa, and, D. D. Metcalfe. 1999. Mast cells and basophils, p. 97117. In J. I. Gallin,, R. Snyderman,, D. T. Fearon,, B. F. Haynes, and, C. Nathan (ed.), Inflammation: Basic Principles and Clinical Correlates, 3rd ed. Lippincott Williams & Wilkins, Philadelphia, Pa.
94. Bradding, P. 1996. Human mast cell cytokines. Clin. Exp. Allergy 26:1319.
95. Lurie, M. B. 1942. Studies on the mechanism of immunity in tuberculosis. The fate of tubercle bacilli ingested by mononuclear phagocytes derived from normal and immunized animals. J. Exp. Med. 75:247268.
96. Mackaness, G. B. 1962. Cellular resistance to infection. J. Exp. Med. 116:381406.
97. Mackaness, G. B. 1964. The immunological basis of acquired cellular resistance. J. Exp. Med. 120:105120.
98. Mackaness, G. B. 1967. The relationship of delayed hypersensitivity to acquired cellular resistance. Br. Med. Bull. 23:5254.
99. Mackaness, G. B., and, R. V. Blanden. 1967. Cellular immunity. Prog. Allergy 11:89140.
100. Mackaness, G. B. 1968. The immunology of antituberculous immunity. Am. Rev. Respir. Dis. 97:337344. (Editorial.)
101. North, R. J. 1974. Cell-mediated immunity and the response to infection, p. 185219. In R. T. McCluskey and, S. Cohen (ed.), Mechanisms of Cell-Mediated Immunity. John Wiley & Sons, Inc., New York, N.Y.
102. Collins, F. M., and, S. G. Campbell. 1982. Immunity to intracellular bacteria. Vet. Immunol. Immunopathol. 3:566.
103. Higuchi, S.,, M. Suga,, A. M. Dannenberg, Jr.,, L. F. Affronti,, I. Azuma,, T. M. Daniel, and, J. P. Petrali. 1981. Persistence of protein, carbohydrate and wax components of tubercle bacilli in dermal BCG lesions. Am. Rev. Respir. Dis. 123:397401.
104. Luster, A. D. 2002. The role of chemokines in linking innate and adaptive immunity. Curr. Opin. Immunol. 14:129135.
105. Bendelac, A., and, D. T. Fearon. 1997. Innate immunity: innate pathways that control acquired immunity. Curr. Opin. Immunol. 9:13.
106. Medzhitov, R., and, C. A. Janeway, Jr. 1997. Innate immunity: impact on the adaptive immune response. Curr. Opin. Immunol. 9:49.
107. Medzhitov, R., and, C. A. Janeway, Jr. 2002. Decoding the patterns of self and nonself by the innate immune system. Science 296:298300.
108. Janeway, C. A., Jr., and, R. Medzhitov. 2002. Innate immune recognition. Annu. Rev. Immunol. 20:197216.
109. Beutler, B., and, J. Hoffmann. 2003. Innate immunity. Editorial overview. Curr. Opin. Immunol. 16:13.
110. van Crevel, R.,, T. H. M. Ottenhoff, and, J. W. M. van der Meer. 2002. Innate immunity to Mycobacterium tuberculosis. Clin. Microbiol. Rev. 15:294309.
111. Uronen-Hansson, H.,, J. Allen,, M. Osman,, G. Squires,, N. Klein, and, R. E. Callard. 2004. Toll-like receptor 2 (TLR2) and TLR4 are present inside human dendritic cells, associated with microtubules and the Golgi apparatus but are not detectable on the cell surface: integrity of micro-tubules is required for interleukin-12 production in response to internalized bacteria. Immunology 111:173178.
112. Krutzik, S. R., and, R. L. Modlin. 2004. The role of Toll-like receptors in combating mycobacteria. Semin. Immunol. 16:3541.
113. Pasare, C., and, R. Medzhitov. 2003. Toll pathway-dependent blockade of CD4+CD8+T cell-mediated suppression by dendritic cells. Science 299:10331036.
114. Kopp, E., and, R. Medzhitov. 2003. Recognition of microbial infection by Toll-like receptors. Curr. Opin. Immunol. 15:396401.
115. Heine, H., and, E. Lien. 2003. Toll-like receptors and their function in innate and adaptive immunity. Int. Arch. Allergy Immunol. 130:180192.
116. Beutler, B.,, K. Hoebe,, X. Du, and, R. J. Ulevitch. 2003. How we detect microbes and respond to them: the Toll-like receptors and their transducers. J. Leukoc. Biol. 74:479485.
117. Auten, R. L.,, R. H. Watkins,, D. L. Shapiro, and, S. Horowitz. 1990. Surfactant apoprotein A (SP-A) is synthesized in airway cells. Am. J. Respir. Cell Mol. Biol. 3:491496.
118. Wu, H.,, A. Kuzmenko,, S. Wan,, L. Schaffer,, A. Weiss,, J. H. Fisher,, K. S. Kim, and, F. X. McCormack. 2003. Surfactant proteins A and D inhibit the growth of Gram-negative bacteria by increasing membrane permeability. J. Clin. Investig. 111:15891602.
119. Wright, J. R. 2003. Pulmonary surfactant: a front line of lung host defense. J. Clin. Investig. 111:14531455.
120. Lenschow, D. J.,, T. L. Walunas, and, J. A. Bluestone. 1996. CD28/B7 system of T cell costimulation. Annu. Rev. Immunol. 14:233258.
121. Roura-Mir, C.,, L. Wang,, T.-Y. Cheng,, I. Matsunaga,, C. C. Dascher,, S. L. Peng,, M. J. Fenton,, C. Kirschning, and, D. B. Moody. 2005. Mycobacterium tuberculosis regulates CD1 antigen presentation pathways through TLR-2. J. Immunol. 175:17581766.
122. Trinchieri, G. 1997. Cytokines acting on or secreted by macrophages during intracellular infection (IL-10, IL-12, IFN-γ). Curr. Opin. Immunol. 9:1723.
123. Trinchieri, G. 1995. Interleukin-12: a proinflammatory cytokine with immunoregulatory functions that bridge innate resistance and antigen-specific adaptive immunity. Annu. Rev. Immunol. 13:251276.
124. Flynn, J. L., and, J. Chan. 2001. Immunology of tuberculosis. Annu. Rev. Immunol. 19:93129.
125. Kaufmann, S. H. E. 2003. Immune response to tuberculosis: experimental animal models. Tuberculosis 83:107111.
126. Rook, G. A. W.,, G. Seah, and, A. Ustianowski. 2001. M. tuberculosis: immunology and vaccination. Eur. Respir. J. 17:537557.
127. Dannenberg, A. M., Jr. 1978. Pathogenesis of pulmonary tuberculosis in man and animals; protection of personnel against tuberculosis, p. 6575. In R. J. Montali (ed.), Mycobacterial Infections of Zoo Animals. Smithsonian Institution Press, Washington, D.C.

Tables

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TABLE 1

Comparisons of the innate and adaptive immune systems a, b

Citation: Dannenberg, Jr. A. 2006. Delayed-Type Hypersensitivity, Cell-Mediated Immunity, and Antibodies in Tuberculosis, p 97-119. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch5

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