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Chapter 21 : Vascular Adhesion Molecules in Tuberculous Lesions

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Abstract:

Vascular adhesion molecules enable host defense cells to leave the bloodstream and enter tuberculous lesions. After the inhalation of tubercle bacilli, Lurie’s resistant rabbits had a larger number of mononuclear cells within developing lesions than did his susceptible rabbits. Therefore, the rapid local accumulation of mononuclear cells seems to be one of the factors associated with resistance to the progress of this disease. Vascular adhesion molecules enable such an accumulation to occur. With immunohistochemical techniques, the author's group evaluated the rise and fall of three major vascular adhesion molecules as rabbit dermal BCG lesions developed and healed. Intercellular adhesion molecule 1 (ICAM- 1) is important for the adherence of polymorphonuclear leukocytes (PMN), monocytes, and lymphocytes to activated vascular endothelium before they emigrate from the bloodstream into sites of inflammation and infection. Vascular cell adhesion molecule 1 (VCAM-1) is a major factor in monocyte, lymphocyte, and eosinophil emigration. Endothelial-leukocyte adhesion molecule 1 (ELAM-1, now called E-selectin) aids the emigration of granulocytes (and some monocytes and T lymphocytes). In tuberculosis, epithelioid cells are macrophages that adhere to one another in an epithelial-like pattern. This adherence seems to be due in part to the ICAM-1 of one macrophage’s binding to its ligand LFA-1 (lymphocyte function-associated antigen 1) (CD11a/CD18) on a neighboring macrophage. ICAM, VCAM, and ELAM are markers for activated vascular endothelial cells. In tuberculous lesions, such activated endothelial cells can capture and present local mycobacterial antigens and therefore may be killed by antigen-specific cytotoxic T lymphocytes.

Citation: Dannenberg, Jr. A. 2006. Vascular Adhesion Molecules in Tuberculous Lesions, p 327-338. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch21
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Figures

Image of FIGURE 1
FIGURE 1

Microvessels in a 9-day rabbit BCG lesion, stained immunohistochemically for ICAM-1 (A) and for VCAM-1 (B). Vessels immunostained for ELAM were similar in appearance. Mouse monoclonal antibodies to rabbit ICAM-1 and VCAM-1, rabbit anti-mouse IgG, counterstained with Giemsa. Magnification, ×475. Reproduced with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Vascular Adhesion Molecules in Tuberculous Lesions, p 327-338. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch21
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Image of FIGURE 2
FIGURE 2

(A) Size (in mm3) of rabbit dermal BCG lesions at various times after their onset. (B) Area of stained microvasculature in such lesions as a percentage of a 1-mm2 area of tissue section. The tissue sections were stained immunohistochemically for von Willebrand (vW) factor (a measure of the total functional microvasculature) and for the adhesion molecules ICAM-1, ELAM-1, and VCAM-1 (1) (see text). The microvasculature was evaluated only in the intact areas of the BCG lesions that were densely infiltrated with inflammatory cells. Normal skin values are shown at zero time. The means and their standard errors are shown. Note that peak levels of adhesion molecules preceded the peak size of the BCG lesions, because the upregulation of these molecules enabled the cell infiltration that caused the BCG lesions to grow in size. To produce this panel, each stained microvessel was circled with the probe of a computerized image analyzer, and its lumen was also circled. The two circled areas were subtracted to provide the area (in mm2) of the vessel wall. Then, the areas occupied by vessel walls in 1 mm2 of tissue section were computed. Reproduced with permission from reference 1. (C) Microvasculature stained for ICAM-1, ELAM-1, and VCAM-1 in BCG lesions as a percentage of a 1-mm2 area of tissue section. This panel confirms the data in panel B, with important 3-day measurements added. Note that ICAM and VCAM peaked at 3 days, suggesting that these adhesion molecules enabled the initial cell infiltration of mononuclear cells (macrophages and lymphocytes) into the BCG lesions. ELAM upregulation was more delayed. The means and their standard errors are shown. Reproduced with permission from reference 21. (D) Vasculature in BCG lesions stained for adhesion molecules as a percentage of the total functional vasculature (vW factor-stained vessels). Presenting the data in this way identifies the upregulation and downregulation of the adhesion molecules more precisely, because changes in the total functional vasculature have been factored out. The means and their standard errors are shown. Reproduced with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Vascular Adhesion Molecules in Tuberculous Lesions, p 327-338. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch21
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Image of FIGURE 3
FIGURE 3

Areas of microvasculature stained immunohistochemically for von Willebrand (vW) factor, ICAM-1, VCAM-1, and ELAM-1, as a percentage of 1-mm2 areas of tissue sections of dermal BCG lesions during the first 5 days. The functional microvasculature (per mm2) (recognized by vW staining) and the three adhesion molecules increased much more rapidly in reinfection lesions (and in tuberculin reactions) than in primary lesions. Most of the functional microvasculature stained for ICAM, but only about half as much stained for VCAM and ELAM (compare the scales on the y axes). In the primary BCG lesions, ELAM-1 was highest at 5 days, but in the reinfection BCG lesions, ELAM was highest at 3 h. The means and their standard errors are shown. Reproduced with permission from reference 22 (where P values can be found).

Citation: Dannenberg, Jr. A. 2006. Vascular Adhesion Molecules in Tuberculous Lesions, p 327-338. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch21
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Image of FIGURE 4
FIGURE 4

A dilated lymphatic vessel in a 1-day acute dermal inflammatory lesion produced in a rabbit by the topical application of 1% sulfur mustard (1). These lesions are markedly edematous at 1 and 2 days, but they are healed in 6 to 10 days. Note the valve in the center of the lymphatic, the nerve on the upper left of the photograph, and the capillary with three erythrocytes below. Numerous leukocytes, especially PMN, are present in the connective tissue. Lymphatics remain patent in rabbit inflammatory lesions (74). In fact, extravasated serum proteins in 1-day sulfur mustard lesions are replaced every 8 h (75). Glycol methacrylate-embedded tissue section (1 to 2 μm thick) stained with Giemsa. Magnification, ×475.

Citation: Dannenberg, Jr. A. 2006. Vascular Adhesion Molecules in Tuberculous Lesions, p 327-338. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch21
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Image of FIGURE 5
FIGURE 5

(A and B) Both photographs show a group of rather mature epithelioid cells (macrophages) surrounding a small necrotic area in a 37-day BCG lesion. The cells in panel A were immunostained for ICAM-1, whereas those in panel B were immunostained for CD11a, which is a component of LFA-1, the ligand on macrophages that binds to ICAM-1. These findings suggest that the ICAM-1–LFA-1 pair is a major contributor to the rather firm cell-cell adherence that characterizes epithelioid cells. Mouse monoclonal antibody to rabbit ICAM and CD11a, biotinylated rabbit anti-mouse IgG, counterstained with methyl green. Magnification, ×200. Reproduced with permission from reference 1.

Citation: Dannenberg, Jr. A. 2006. Vascular Adhesion Molecules in Tuberculous Lesions, p 327-338. In Pathogenesis of Human Pulmonary Tuberculosis. ASM Press, Washington, DC. doi: 10.1128/9781555815684.ch21
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References

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1. Abe, Y.,, K. Sugisaki, and, A. M. Dannenberg, Jr. 1996. Rabbit vascular endothelial adhesion molecules: ELAM-1 is most elevated in acute inflammation, whereas VCAM-1 and ICAM-1 predominate in chronic inflammation. J. Leukoc. Biol. 60:692703.
2. Cotran, R. S., and, T. Mayadas-Norton. 1998. Endothelial adhesion molecules in health and disease. Pathol. Biol. (Paris) 46:164170.
3. Pober, J. S., and, R. S. Cotran. 1990. The role of endothelial cells in inflammation. Transplantation 50:537544.
4. Pigott, R., and, C. Power. 1993. The Adhesion Molecule Facts Book. Academic Press, Inc., San Diego, Calif.
5. Majno, G., and, I. Joris. 2004. Cells, Tissues, and Disease: Principles of General Pathology, 2nd ed., p. 403428. Oxford University Press, New York, N.Y.
6. Norris, P.,, R. N. Poston,, D. S. Thomas,, M. Thornhill,, J. Hawk, and, D. O. Haskard. 1991. The expression of endothelial leukocyte adhesion molecule-1 (ELAM-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in experimental cutaneous inflammation: a comparison of ultraviolet B erythema and delayed hypersensitivity. J. Investig. Dermatol. 96:763770.
7. Kupper, T. S. 1990. Immune and inflammatory processes in cutaneous tissues: mechanisms and speculations. J. Clin. Investig. 86:17831789.
8. Tsuruta, J.,, K. Sugisaki,, A. M. Dannenberg, Jr.,, T. Yoshimura,, Y. Abe, and, P. Mounts. 1996. The cytokines NAP-1 (IL-8), MCP-1, IL-1β, and GRO in rabbit inflammatory skin lesions produced by the chemical irritant sulfur mustard. Inflammation 20:293318.
9. Bevilacqua, M. P., and, R. M. Nelson. 1993. Selectins. J. Clin. Investig. 91:379387.
10. McEver, R. P. 1994. Selectins. Curr. Opin. Immunol. 6:7584.
11. Zack, O. M.,, A. Ben-Baruch, and, J. J. Oppenheim. 1996. Chemokines: progress toward identifying molecular targets for therapeutic agents. Trends Biotechnol. 14:4651.
12. Bacon, K. B., and, T. J. Schall. 1996. Chemokines as mediators of allergic inflammation. Int. Arch. Allergy Immunol. 109:97109.
13. Springer, T. A. 1990. Adhesion receptors of the immune system. Nature 346:425434.
14. Wawryk, S. O.,, J. R. Novotny,, I. P. Wicks,, D. Wilkinson,, D. Maher,, E. Salvaris,, K. Welch,, J. Fecondo, and, A. W. Boyd. 1989. The role of LFA-1/ICAM-1 interaction in human leukocyte homing and adhesion. Immunol. Rev. 108:135161.
15. Courtade, E. T.,, T. Tsuda,, C. R. Thomas, and, A. M. Dannenberg, Jr. 1975. Capillary density in developing and healing tuberculous lesions produced by BCG in rabbits. A quantitative study. Am. J. Pathol. 78:243260.
16. Eddy, H. A., and, G. W. Casarett. 1968. Intestinal vascular changes in the acute radiation intestinal syndrome, p. 385395. In M. F. Sullivan (ed.), Monographs on Nuclear Medicine and Biology, no. 1. Gastrointestinal Radiation Injury. Excerpta Medica Foundation, Amsterdam, The Netherlands.
17. Wagner, D. D., and, R. Bonfanti. 1991. von Willebrand factor and the endothelium. Mayo Clin. Proc. 66:621627.
18. Jaffe, E. A. 1987. Cell biology of endothelial cells. Hum. Pathol. 18:234239.
19. Lollar, P.,, D.C. Hill-Eubanks, and, C. G. Parker. 1988. Association of the Factor VIII light chain with von Willebrand factor. J. Biol. Chem. 263:1045110455.
20. Blann, A. D. 1993. Is raised von Willebrand factor a marker of endothelial cell damage? Med. Hypotheses 41:419424.
21. Blann, A. D. 1993. von Willebrand factor as a marker of injury to the endothelium in inflamma-tory vascular disease. J. Rheumatol. 20:14691471. (Editorial.)
22. 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.
23. 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.
24. Norris, P.,, R. N. Poston,, D. S. Thomas,, M. Thornhill,, J. Hawk, and, D. O. Haskard. 1991. The expression of endothelial leukocyte adhesion molecule-1 (ELAM-1), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in experimental cutaneous inflammation: a comparison of ultraviolet B erythema and delayed hypersensitivity. J. Investig. Dermatol. 96:763770.
25. Silber, A.,, W. Newman,, K. A. Reimann,, E. Hendricks,, D. Walsh, and, D. J. Ringler. 1994. Kinetic expression of endothelial adhesion molecules and relationship to leukocyte recruitment in two cutaneous models of inflammation. Lab. Investig. 70:163175.
26. Schleiffenbaum, B., and, J. Fehr. 1996. Regulation and selectivity of leukocyte emigration. J. Lab. Clin. Med. 127:151168.
27. Chuluyan, H. E.,, L. Osborn,, R. Lobb, and, A. C. Issekutz. 1995. Domains 1 and 4 of vascular cell adhesion molecule-1 (CD106) both support very late activation antigen-4 (CD49d/CD29)-dependent monocyte transendothelial migration. J. Immunol. 155:31353144.
28. Rice, G. E.,, J. M. Munro, and, M. P. Bevilacqua. 1990. Inducible cell adhesion molecule 110 (INCAM-110) is an endothelial receptor for lymphocytes. A CD11/CD18-independent adhesion mechanism. J. Exp. Med. 171:13691374.
29. Carlos, T. M.,, B. R. Schwartz,, N. L. Kovach,, E. Yee,, M. Rosso,, L. Osborn,, G. Chi-Rosso,, B. Newman,, R. Lobb, and, J. M. Harlan. 1990. Vascular cell adhesion molecule-1 mediates lymphocyte adherence to cytokine-activated cultured human endothelial cells. Blood 76:965970.
30. Kuijpers, T. W., and, J. M. Harlan. 1993. Monocyte-endothelial interactions: insights and questions. J. Lab. Clin. Med. 122:641651.
31. Chuluyan, H. E., and, A. C. Issekutz. 1993. VLA-4 integrin can mediate CD11/CD18-independent transendothelial migration of human monocytes. J. Clin. Investig. 92:27682777.
32. Verdegaal, E. M. E.,, H. Beekhuizen,, I. Blok-land, and, R. van Furth. 1993. Increased adhesion of human monocytes to IL-4-stimulated human venous endothelial cells via CD11/CD18, and very late antigen-4 (VLA-4)/vascular cell adhesion molecule-1 (VCAM-1)-dependent mechanisms. Clin. Exp. Immunol. 93:292298.
33. Silber, A.,, W. Newman,, V. G. Sasseville,, D. Pauley,, D. Beall,, D. G. Walsh, and, D. J. Ringler. 1995. Recruitment of lymphocytes during cutaneous delayed hypersensitivity in nonhuman primates is dependent on E-selectin and VCAM-1. J. Clin. Investig. 93:15541563.
34. Alon, R.,, P. D. Kassner,, M. W. Carr,, E. B. Finger,, M. E. Hemler, and, T. A. Springer. 1995. The integrin VLA-4 supports tethering and rolling in flow on VCAM-1. J. Cell Biol. 128:12431253.
35. Issekutz, T. B., and, A. C. Issekutz. 1991. T lymphocyte migration to arthritic joints and dermal inflammation in the rat: differing migration patterns and the involvement of VLA-4. Clin. Immunol. Immunopathol. 61:436447.
36. Carlos, T. M., and, J. M. Harlan. 1994. Leukocyte-endothelial adhesion molecules. Blood 84:20682101.
37. Adams, D. H., and, S. Shaw. 1994. Leucocyte-endothelial interactions and regulation of leucocyte migration. Lancet 343:831836.
38. Olofsson, A. M.,, K.-E. Arfors,, L. Ramezani,, B. A. Wolitzky,, E. C. Butcher, and, U. H. von Andrian. 1994. E-selectin mediates leukocyte rolling interleukin-1-treated rabbit mesentery venules. Blood 84:27492758.
39. Munro, J. M.,, J. S. Pober, and, R. S. Cotran. 1991. Recruitment of neutrophils in the local endotoxin response: association with de novo endothelial expression of endothelial leukocyte adhesion molecule-1. Lab. Investig. 64:295299.
40. Butcher, E. C. 1991. Leukocyte-endothelial cell recognition: three (or more) steps to specificity and diversity. Cell 67:10331036.
41. Luscinskas, F. W.,, G. S. Kansas,, H. Ding,, P. Pizcueta,, B. E. Schleiffenbaum,, T. F. Tedder, and, M. A. Gimbrone, Jr. 1994. Monocyte rolling, arrest and spreading on IL-4-activated vascular endothelium under flow is mediated via sequential action of L-selectin, β1-integrins, and β2-integrins. J. Cell Biol. 125:14171427.
42. Picker, L. J.,, T. K. Kishimoto,, C. W. Smith,, R. A. Warnock, and, E. C. Butcher. 1991. ELAM-1 is an adhesion molecule for skin-homing T cells. Nature 349:796799.
43. Schleimer, R. P.,, M. Ebisawa,, S. N. Georas, and, B. S. Bochner. 1994. The role of adhesion molecules and cytokines in eosinophil recruitment, p. 99114. In G. J. Gleich and, A. B. Kay (ed.), Eosinophils in Allergy and Inflammation. Marcel Dekker, Inc., New York, N.Y.
44. Sharar, S. R.,, R. K. Winn, and, J. M. Harlan. 1995. The adhesion cascade and anti-adhesion therapy: an overview. Springer Semin. Immunopathol. 16:359378.
45. Lukacs, N. W.,, R. M. Strieter,, V. Elner,, H. L. Evanoff,, M. D. Burdick, and, S. L. Kunkel. 1995. Production of chemokines, interleukin-8 and monocyte chemoattractant protein-1, during monocyte: endothelial cell interactions. Blood 86:27672773.
46. Albelda, S. M.,, C. W. Smith, and, P. A. Ward. 1994. Adhesion molecules and inflammatory injury. FASEB J. 8:504512.
47. Hogg, N., and, C. Berlin. 1995. Structure and function of adhesion receptors in leukocyte trafficking. Immunol. Today 16:327330.
48. Duperray, A.,, A. Mantovani,, M. Introna, and, E. Dejana. 1995. Endothelial cell regulation of leukocyte infiltration in inflammatory tissues. Mediat. Inflamm. 4:322330.
49. Chuluyan, H. E., and, A. C. Issekutz. 1995. Alpha 4-integrin-dependent emigration of monocytes. Springer Semin. Immunopathol. 16:391404.
50. Issekutz, A. C.,, H. E. Chuluyan, and, N. Lopes. 1995. CD11/CD18-independent transendothelial migration of human polymorphonuclear leukocytes and monocytes: involvement of distinct and unique mechanisms. J. Leukoc. Biol. 57:553561.
51. Murphy, J. F., and, J. L. McGregor. 1994. Two sites on P-selectin (the lectin and epidermal growth factor-like domains) are involved in the adhesion of monocytes to thrombin-activated endothelial cells. Biochem. J. 303:619624.
52. Meng, H.,, M. G. Tonnesen,, M. J. Marchese,, R. A. F. Clark,, W. F. Bahou, and, B. L. Gruber. 1995. Mast cells are potent regulators of endothelial cell adhesion molecule ICAM-1 and VCAM-1 expression. J. Cell. Physiol. 165:4053.
53. Pugin, J.,, R. J. Ulevitch, and, P. S. Tobias. 1995. Tumor necrosis factor-α and interleukin-1β mediate human endothelial cell activation in blood at low endotoxin concentrations. J. Inflamm. 45:4955.
54. McEver, R. P. 1991. Selectins: novel receptors that mediate leukocyte adhesion during inflammation. Thromb. Haemost. 65:223228.
55. Garcia, J. G. N.,, F. M. Pavalko, and, C. E. Patterson. 1995. Vascular endothelial cell activation and permeability responses to thrombin. Blood Coagul. Fibrinolysis 6:609626.
56. Qi, J., and, D. L. Kreutzer. 1995. Fibrin activation of vascular endothelial cells: induction of IL-8 expression. J. Immunol. 155:867876.
57. Nathan, C., and, M. Sporn. 1991. Cytokines in context. J. Cell Biol. 113:981986.
58. Kuijpers, T. W. 1995. Pathophysiological aspects of VLA-4 interactions and possibilities for therapeutical interventions. Springer Semin. Immunopathol. 16:379389.
59. Buck, C. A. 1995. What’s potentially more effective than a Roto-Rooter and less toxic than Drano? Anti-adhesions mimetics! J. Clin. Invest. 95:24312432.
60. Hamman, A. (ed.). 1997. Adhesion Molecules and Chemokines in Lymphocyte Trafficking. Harwood Academic Publishers, Amsterdam, The Netherlands.
61. Pober, J. S., and, R. S. Cotran. 1991. Immuno-logic interactions of T lymphocytes with vascular endothelium. Adv. Immunol. 50:261302.
62. Smith, R. E.,, C. M. Hogaboam,, R. M. Strieter,, N. W. Lukacs, and, S. L. Kunkel. 1997. Cell-to-cell and cell-to-matrix interactions mediate chemokine expression: an important component of the inflammatory lesion. J. Leukoc. Biol. 62:612619.
63. Bochner, B. S. 1997. Cellular adhesion and its antagonism. J. Allergy Clin. Immunol. 100:581585.
64. Cybulsky, M. I., and, M. A. Gimbrone, Jr. 1991. Endothelial expression of a mononuclear leukocyte adhesion molecule during atherogenesis. Science 251:788791.
65. Richardson, M.,, S. J. Hadcock,, M. DeReske, and, M. I. Cybulsky. 1994. Increased expression in vivo of VCAM-1 and E-selectin by the aortic endothelium of normolipemic and hyperlipemic diabetic rabbits. Arterioscler. Thromb. 14:760769.
66. Tanaka, H.,, G. K. Sukhova,, S. J. Swanson,, M. I. Cybulsky,, F. J. Schoen, and, P. Libby. 1994. Endothelial and smooth muscle cells express leukocyte adhesion molecules heterogeneously during acute rejection of rabbit cardiac allografts. Am. J. Pathol. 144:938951.
67. Molossi, S.,, M. Elices,, T. Arrhenius,, R. Diaz,, C. Coulber, and, M. Rabinovitch. 1995. Blockade of very late antigen-4 integrin binding to fibronectin with connecting segment-1 peptide reduces accelerated coronary arteriopathy in rabbit cardiac allografts. J. Clin. Investig. 95:26012610.
68. Pober, J. S.,, M. A. Gimbrone, Jr.,, R. S. Cotran,, C. S. Reiss,, S. J. Burakoff,, W. Fiers, and, K. A. Ault. 1983. Ia expression by vascular endothelium is inducible by activated T cells and by human interferon gamma. J. Exp. Med. 157:13391353.
69. Collins, T.,, A. J. Korman,, C. T. Wake,, J. M. Boss,, D. J. Kappes,, W. Fiers,, K. A. Ault,, M. A. Gimbrone, Jr.,, J. L. Strominger, and, J. S. Pober. 1984. Immune interferon activates multiple class II major histocompatibility complex genes and the associated invariant chain gene in human endothelial cells and dermal fibroblasts. Proc. Natl. Acad. Sci. USA 81:49174921.
70. Pober, J. S.,, T. Collins,, M. A. Gimbrone, Jr.,, P. Libby, and, C. S. Reiss. 1986. Overview: inducible expression of class II major histocompatibility complex antigens and the immunogenicity of vascular endothelium. Transplantation 41:141146.
71. Turner, R. R.,, J. H. Beckstead,, R. A. Warnke, and, G. S. Wood. 1987. Endothelial cell phenotypic diversity: in situ demonstration of immunologic and enzymatic heterogeneity that correlates with specific morphologic subtypes. Am. J. Clin. Pathol. 87:569575.
72. Dannenberg, A. M., Jr. 1993. Pathogenesis of pulmonary tuberculosis. Hosp. Pract. 28:3340 (Off. ed. 51–58).
73. 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. ASM Press, Washington, D.C.
74. Pasqualini, R.,, D. M. McDonald, and, W. Arap. 2001. Vascular targeting and antigen presentation. Nat. Immunol. 2:567568.
75. Weiss, H. J. 1975. Platelet physiology and abnormalities of platelet function. N. Engl. J. Med. 293:531541.
76. Lurie, M. B. 1964. Resistance to Tuberculosis: Experimental Studies in Native and Acquired Defensive Mechanisms. Harvard University Press, Cambridge, Mass.
77. Harada, S.,, A. M. Dannenberg, Jr.,, A. Kajiki,, K. Higuchi,, F. Tanaka, and, P. J. Pula. 1985. Inflammatory mediators and modulators released in organ culture from rabbit skin lesions produced in vivo by sulfur mustard. II. Evans blue dye experiments that determined the rates of entry and turnover of serum protein in developing and healing lesions. Am. J. Pathol. 121:2838.

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