Involvement of both 'allergic' and 'autoimmune' mechanisms in EAE, MS and other autoimmune diseases

Trends in Immunology

Volumn 24, Issue 9, 2003, Pages 479-484

  Pedotti, Rosetta ^a   De Voss, Jason J ^b   Steinman, Lawrence ^b   Galli, Stephen J ^c  

^a DEPARTMENT OF NEUROSURGERY   (Italy)

^b STANFORD UNIVERSITY MEDICAL CENTER   (United States)

^c STANFORD UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

FC RECEPTOR; GAMMA INTERFERON; HISTAMINE H1 RECEPTOR; HISTAMINE H2 RECEPTOR; IMMUNOGLOBULIN E; IMMUNOGLOBULIN E ANTIBODY; IMMUNOGLOBULIN G1; INTERLEUKIN 4; MYELIN PROTEIN; OSTEOPONTIN; PEPTIDE; PROTEOLIPID; THROMBOCYTE ACTIVATING FACTOR; TRYPTASE; TUMOR NECROSIS FACTOR ALPHA;

ALLERGIC ENCEPHALOMYELITIS; ALLERGIC REACTION; ALLERGY; ANAPHYLAXIS; AUTOIMMUNE DISEASE; AUTOIMMUNITY; CENTRAL NERVOUS SYSTEM DISEASE; CYTOKINE PRODUCTION; GENE EXPRESSION REGULATION; GENE FUNCTION; GENE OVEREXPRESSION; HELPER CELL; HUMAN; IMMUNE RESPONSE; IMMUNE SYSTEM; MAST CELL; MULTIPLE SCLEROSIS; NONHUMAN; PATHOGENESIS; PEMPHIGOID; REVIEW; RHEUMATOID ARTHRITIS; TH1 CELL; TH2 CELL;

EID: 0042380071     PISSN: 14714906     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1471-4906(03)00233-3     Document Type: Article

References (70)

1. Mosmann T.R., et al. Two types of murine helper T cell clone. I. Definition according to profiles of lymphokine activities and secreted proteins. J. Immunol. 136:1986;2348-2357.
2. Mosmann T.R., Coffman R.L. TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties. Annu. Rev. Immunol. 7:1989;145-173.
3. + T-cell subsets: regulation of differentiation and function. Res. Immunol. 142:1991;7-9.
4. Stene L.C., Nafstad P. Relation between occurrence of type 1 diabetes and asthma. Lancet. 357:2001;607-608.
5. Yazdanbakhsh M., et al. Allergy, parasites, and the hygiene hypothesis. Science. 296:2002;490-494.
6. Bach J.F. The effect of infections on susceptibility to autoimmune and allergic diseases. N. Engl. J. Med. 347:2002;911-920.
7. Steinman L. Multiple sclerosis: a two-stage disease. Nat. Immunol. 2:2001;762-764.
8. Steinman L. Optic neuritis, a new variant of experimental encephalomyelitis, a durable model for all seasons, now in its seventieth year. J. Exp. Med. 197:2003;1065-1071.
9. Zamvil S.S., Steinman L. Diverse targets for intervention during inflammatory and neurodegenerative phases of multiple sclerosis. Neuron. 38:2003;685-688.
10. Steinman L., Zamvil S. Transcriptional analysis of targets in multiple sclerosis. Nat. Rev. Immunol. 3:2003;483-492.
11. Martino G., et al. The ependymal route to the CNS: an emerging gene-therapy approach for MS. Trends Immunol. 22:2001;483-490.
12. Lafaille J.J., et al. Myelin basic protein-specific T helper 2 (Th2) cells cause experimental autoimmune encephalomyelitis in immunodeficient hosts rather than protect them from the disease. J. Exp. Med. 186:1997;307-312.
13. Gladue R.P., et al. Inhibition of leukotriene B4-receptor interaction suppresses eosinophil infiltration and disease pathology in a murine model of experimental allergic encephalomyelitis. J. Exp. Med. 183:1996;1893-1898.
14. Pedotti R., et al. An unexpected version of horror autotoxicus: anaphylactic shock to a self-peptide. Nat. Immunol. 2:2001;216-222.
15. Pedotti R., et al. Multiple elements of the allergic arm of the immune response modulate autoimmune demyelination. Proc. Natl. Acad. Sci. U. S. A. 100:2003;1867-1872.
16. Liu E., et al. Anti-peptide autoantibodies and fatal anaphylaxis in NOD mice in response to insulin self-peptides B:9-23 and B:13-23. J. Clin. Invest. 110:2002;1021-1027.
17. Pedotti R., et al. Severe anaphylactic reactions to glutamic acid decarboxylase (GAD) self peptides in NOD mice that spontaneously develop autoimmune type 1 diabetes mellitus. BMC Immunol. 4:2003;2.
18. Begolka W.S., et al. Differential expression of inflammatory cytokines parallels progression of central nervous system pathology in two clinically distinct models of multiple sclerosis. J. Immunol. 161:1998;4437-4446.
19. Galli S.J., Lantz C.S. Allergy. Paul W.E. Fundamental Immunology. 1999;1137-1184 Lippincott-Raven Press.
20. Abbas A.K., et al. Functional diversity of helper T lymphocytes. Nature. 383:1996;787-793.
21. Ichikawa M., et al. IgG subclass switching is associated with the severity of experimental autoimmune encephalomyelitis induced with myelin oligodendrocyte glycoprotein peptide in NOD mice. Cell. Immunol. 191:1999;97-104.
22. Robbie-Ryan M., et al. Both activating and inhibitory Fc receptors expressed on mast cells regulate experimental allergic encephalomyelitis disease severity. J. Immunol. 170:2003;1630-1634.
23. Tisch R., et al. Immune response to glutamic acid decarboxylase correlates with insulitis in non-obese diabetic mice. Nature. 366:1993;72-75.
24. + cells. Adv. Immunol. 53:1993;1-29.
25. Gordon J.R., et al. Mast cells as a source of multifunctional cytokines. Immunol. Today. 11:1990;458-464.
26. Brown M., et al. Mechanisms underlying mast cell influence on EAE disease course. Mol. Immunol. 38:2002;1373.
27. Kawakami T., Galli S.J. Regulation of mast-cell and basophil function and survival by IgE. Nat. Rev. Immunol. 2:2002;773-786.
28. Secor V.H., et al. Mast cells are essential for early onset and severe disease in a murine model of multiple sclerosis. J. Exp. Med. 191:2000;813-822.
29. Zappulla J.P., et al. Mast cells: new targets for multiple sclerosis therapy? J. Neuroimmunol. 131:2002;5-20.
30. Theoharides T.C. Mast cells: the immune gate to the brain. Life Sci. 46:1990;607-617.
31. Benoist C., Mathis D. Mast cells in autoimmune disease. Nature. 420:2002;875-878.
32. Lock C., et al. Gene-microarray analysis of multiple sclerosis lesions yields new targets validated in autoimmune encephalomyelitis. Nat. Med. 8:2002;500-508.
33. Ibrahim M.Z., et al. The mast cells of the multiple sclerosis brain. J. Neuroimmunol. 70:1996;131-138.
34. Robbie-Ryan M., Brown M. The role of mast cells in allergy and autoimmunity. Curr. Opin. Immunol. 14:2002;728-733.
35. Abdul-Majid K.B., et al. Fc receptors are critical for autoimmune inflammatory damage to the central nervous system in experimental autoimmune encephalomyelitis. Scand. J. Immunol. 55:2002;70-81.
36. Chen R., et al. Mast cells play a key role in neutrophil recruitment in experimental bullous pemphigoid. J. Clin. Invest. 108:2001;1151-1158.
37. Lee D.M., et al. Mast cells: a cellular link between autoantibodies and inflammatory arthritis. Science. 297:2002;1689-1692.
38. Linthicum D.S. Development of acute autoimmune encephalomyelitis in mice: factors regulating the effector phase of the disease. Immunobiology. 162:1982;211-220.
39. Dietsch G.N., Hinrichs D.J. The role of mast cells in the elicitation of experimental allergic encephalomyelitis. J. Immunol. 142:1989;1476-1481.
40. Dimitriadou V., et al. Hydroxyzine inhibits experimental allergic encephalomyelitis (EAE) and associated brain mast cell activation. Int. J. Immunopharmacol. 22:2000;673-684.
41. Yamatodani A., et al. Tissue distribution of histamine in a mutant mouse deficient in mast cells: clear evidence for the presence of non-mast-cell histamine. Biochem. Pharmacol. 31:1982;305-309.
42. Sugimoto K., et al. Brain histaminergic system in mast cell-deficient (Ws/Ws) rats: histamine content, histidine decarboxylase activity, and effects of (S) α-fluoromethylhistidine. J. Neurochem. 65:1995;791-797.
43. Huang C., et al. Regulation and function of mast cell proteases in inflammation. J. Clin. Immunol. 18:1998;169-183.
44. Schwartz L.B. Tryptase, a mediator of human mast cells. J. Allergy Clin. Immunol. 86:1990;594-598.
45. Schilling L., Wahl M. Opening of the blood-brain barrier during cortical superfusion with histamine. Brain Res. 653:1994;289-296.
46. Yong T., et al. Histamine-induced microvascular leakage in pial venules: differences between the SJL/J and BALB/c inbred strains of mice. J. Neurotrauma. 11:1994;161-171.
47. Sharma H.S., et al. Changes in blood-brain barrier and cerebral blood flow following elevation of circulating serotonin level in anesthetized rats. Brain Res. 517:1990;215-223.
48. Sibson N.R., et al. TNF-α reduces cerebral blood volume and disrupts tissue homeostasis via an endothelin- and TNFR2-dependent pathway. Brain. 125:2002;2446-2459.
49. Del Maschio A., et al. Leukocyte recruitment in the cerebrospinal fluid of mice with experimental meningitis is inhibited by an antibody to junctional adhesion molecule (JAM). J. Exp. Med. 190:1999;1351-1356.
50. Linthicum D.S., Frelinger J.A. Acute autoimmune encephalomyelitis in mice II. Susceptibility is controlled by the combination of H-2 and histamine sensitization genes. J. Exp. Med. 156:1982;31-40.
51. Black W.J., et al. ADP-ribosyltransferase activity of pertussis toxin and immunomodulation by Bordetella pertussis. Science. 240:1988;656-659.
52. Meeker N.D., et al. Physical mapping of the autoimmune disease susceptibility locus, Bphs: co-localization with a cluster of genes from the TNF receptor superfamily on mouse chromosome 6. Mamm. Genome. 10:1999;858-863.
53. Blankenhorn E.P., et al. Genetic analysis of the influence of pertussis toxin on experimental allergic encephalomyelitis susceptibility: an environmental agent can override genetic checkpoints. J. Immunol. 164:2000;3420-3425.
54. Teuscher C. Experimental allergic orchitis in mice. II. Association of disease susceptibility with the locus controlling Bordetella pertussis-induced sensitivity to histamine. Immunogenetics. 22:1985;417-425.
55. Ma R.Z., et al. Identification of Bphs, an autoimmune disease locus, as histamine receptor H1. Science. 297:2002;620-623.
56. Jutel M., et al. Histamine regulates T-cell and antibody responses by differential expression of H1 and H2 receptors. Nature. 413:2001;420-425.
57. Strait R.T., et al. Pathways of anaphylaxis in the mouse. J. Allergy Clin. Immunol. 109:2002;658-668.
58. Park T.S., et al. Platelet-activating factor mediates ischemia-induced leukocyte-endothelial adherence in newborn pig brain. J. Cereb. Blood Flow Metab. 19:1999;417-424.
59. Kumar R., et al. Production and effects of platelet-activating factor in the rat brain. Biochim. Biophys. Acta. 963:1988;375-383.
60. Montrucchio G., et al. Role of platelet-activating factor in cardiovascular pathophysiology. Physiol. Rev. 80:2000;1669-1699.
61. Callea L., et al. Platelet activating factor is elevated in cerebral spinal fluid and plasma of patients with relapsing-remitting multiple sclerosis. J. Neuroimmunol. 94:1999;212-221.
62. Qi J.C., et al. IL-16 regulation of human mast cells/basophils and their susceptibility to HIV-1. J. Immunol. 168:2002;4127-4134.
63. Schwartz L.B. Clinical utility of tryptase levels in systemic mastocytosis and associated hematologic disorders. Leuk. Res. 25:2001;553-562.
64. Imamura T., et al. Induction of vascular permeability enhancement by human tryptase: dependence on activation of prekallikrein and direct release of bradykinin from kininogens. Lab. Invest. 74:1996;861-870.
65. Molino M., et al. Interactions of mast cell tryptase with thrombin receptors and PAR-2. J. Biol. Chem. 272:1997;4043-4049.
66. Huang C., et al. The tryptase, mouse mast cell protease 7, exhibits anticoagulant activity in vivo and in vitro due to its ability to degrade fibrinogen in the presence of the diverse array of protease inhibitors in plasma. J. Biol. Chem. 272:1997;31885-31893.
67. Sobel R.A., Mitchell M.E. Fibronectin in multiple sclerosis lesions. Am. J. Pathol. 135:1989;161-168.
68. Rozniecki J.J., et al. Elevated mast cell tryptase in cerebrospinal fluid of multiple sclerosis patients. Ann. Neurol. 37:1995;63-66.
69. Miyajima I., et al. Systemic anaphylaxis in the mouse can be mediated largely through IgG1 and FcγRIII. Assessment of the cardiopulmonary changes, mast cell degranulation, and death associated with active or IgE- or IgG1-dependent passive anaphylaxis. J. Clin. Invest. 99:1997;901-914.
70. Jutel M., et al. Histamine upregulates Th1 and downregulates Th2 responses due to different patterns of surface histamine 1 and 2 receptor expression. Int. Arch. Allergy Immunol. 124:2001;190-192.