Mediators of inflammation

Current Opinion in Immunology

Volumn 9, Issue 6, 1997, Pages 851-857

  Sacca, Rosalba ^a   Cuff, Carolyn A ^a   Ruddle, Nancy H ^a  

^a YALE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CHEMOKINE; CYTOKINE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; AUTOIMMUNE DISEASE; CONTROLLED STUDY; GENETIC ENGINEERING; INFLAMMATION; LYMPHOID ORGAN; MEDIATOR; MOUSE; NONHUMAN; REVIEW; T LYMPHOCYTE; TRANSGENIC MOUSE;

EID: 0031459822     PISSN: 09527915     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0952-7915(97)80189-6     Document Type: Article

References (58)

1. Picker LJ, Butcher EC: Physiological and molecular mechanisms of lymphocyte homing. Annu Rev Immunol 1992, 10:551-591.
2. Paul WE, Seder RA: Lymphocyte responses and cytokines. Cell 1994, 76:241-251.
3. Schall TJ, Bacon KB: Chemokines, leukocyte trafficking, and inflammation. Curr Opin Immunol 1994, 6:865-873.
4. Benveniste EN: Inflammatory cytokines within the central nervous system: sources, function, and mechanism of action. Am J Physiol 1992, 263:C1-C16.
5. Ferber I, Brocke S, Taylor-Edwards C, Ridway W, Dinisco C, Steinman L, Dalton D, Fathman C: Mice with a disrupted IFN-γ gene are susceptible to the induction of experimental autoimmune encephalomyelitis (EAE). J Immunol 1996, 156:5-7. In contrast to the expected result that IFN-γ is an inflammatory mediator, this paper shows that mice with a targeted disruption of the IFN-γ gene when crossed with an EAE-susceptible mouse strain develop EAE.
6. Willenborg D, Fordham S, Bernard CCA, Cowden WB, Ramshaw IA: IFN-γ plays a critical down-regulatory role in the induction and effector phase of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis. J Immunol 1996, 157:3223-3227. This paper shows that mice that lack the gene coding for the ligand-binding chain of the receptor for IFN-γ develop EAE with high morbidity and mortality, suggesting an important role of IFN-γ in down-regulation of EAE.
7. Selmaj K, Raine CS, Cannella B, Brosnan CF: Identification of lymphotoxin and tumor necrosis factor in multiple sclerosis lesions. J Clin Invest 1991, 87:949-954.
8. Powell MB, Mitchell D, Lederman J, Buckmeier J, Zamvil SS, Graham M, Ruddle NH, Steinman L: Lymphotoxin and tumor necrosis factor-alpha production by myelin basic protein-specific T cell clones correlates with encephalitogenicity. Int Immunol 1990, 2:539-544.
9. Ruddle NH, Bergman CM, McGrath KM, Lingenheld EG, Grunnet ML, Padula SJ, Clark RB: An antibody to lymphotoxin and tumor necrosis factor prevents transfer of experimental allergic encephalomyelitis. J Exp Med 1990, 172:1193-1200.
10. Willenborg DO, Fordham SA, Cowden WB, Ramshaw IA: Cytokines and murine autoimmune encephalomyelitis: inhibition or enhancement of disease with antibodies to select cytokines, or by delivery of exogenous cytokines using a recombinant vaccinia virus system. Scand J Immunol 1995, 41:31-41.
11. Taupin VR, Renno T, Bourbonniere L, Peterson AC, Rodriguez M, Owens T: Increased severity of experimental autoimmune encephalomyelitis, chronic macrophage/microglial reactivity, and demyelination in transgenic mice producing tumor necrosis factor-alpha in the central nervous system. Eur J Immunol 1997, 27:905-913.
12. Frei K, Eugster H-P, Bopst M, Constantinescu C, Lavi E, Fontana A: Tumor necrosis factor α and lymphotoxin α are not required for induction of acute experimental autoimmune encephalomyelitis. J Exp Med 1997, 185:2177-2182.
13. Suen WE, Bergman CM, Hjelmstrom P, Ruddle NH: A critical role for lymphotoxin in experimental allergic encephalomyelitis. J Exp Med 1997, 186:1233-1240.
14. Grewal IS, Grewal KD, Wong FS, Picarella DE, Janeway CA Jr, Flavell RA: Local expression of transgene encoded TNFα in islets prevents autoimmune diabetes in nonobese diabetic (NOD) mice by preventing the development of auto-reactive islet-specific T cells. J Exp Med 1996, 184:1963-1974.
15. Cope A, Liblau R, Yang X-D, Congia M, Laudanna C, Schreiber R, Probert L, Kollias G, McDevitt H: Chronic tumor necrosis factor alters T cell responses by attenuating T cell receptor signaling. J Exp Med 1997, 185:1573-1584.
16. Van Deventer S: Tumour necrosis factor and Crohn's disease. Gastroenterology 1995, 109:443-448.
17. Targan S, Rutgeerts P, Hanauer S, Van Deventer S, Mayer L, Present DH, Braakman TAJ, Woody JN: A multicenter trial of anti-tumor necrosis factor (TNF) antibody (cA2) for treatment of patients with active Crohn's disease [abstract]. Gastroenterology 1996, 110:A1026.
18. Plevy SE, Carramanzana NM, Deem RL, Woody JN, Targan SR: Clinical improvement in Crohn's disease patients treated with anti-TNFα correlates with downregulated mucosal Th1 responses [abstract]. Gastroenterology 1996, 110:A993.
19. Neurath M, Fuss I, Pasparakis M, Alexopoulou L, Haralambous S, K-H Meyer zum Büsschenfelde, Strober W, Kollias G: Predominant pathogenic role of tumor necrosis factor in experimental colitis in mice. Eur J Immunol 1997, 27:1743-1750.
20. Mori L, Iselin S, De Libero G, Lesslauer W: Attenuation of collagen-induced arthritis in 55-kDa TNF receptor type 1 (TNFR1)-IgG1-treated and TNFR1-deficient mice. J Immunol 1996, 157:3178-3182. This paper shows that TNFR1-IgG, if given at the appropriate time (during the late initiation phase) of the arthritic process, is sufficient for CIA prevention. The study also shows that mice lacking TNFR1 have reduced incidence and severity of CIA, suggesting that TNFR1 has an important role but other mechanisms are also involved.
21. Cohen J, Carlet J: INTERSEPT: an international, multicenter, placebo-controlled trial of monoclonal antibody to human tumor necrosis factor-α in patients with sepsis. Crit Care Med 1996, 24:1431-1439.
22. Reinhart K, Wiegand-Lohnert C, Grimminger F, Kaul M, Withington S, Treacher D, Eckart J, Willattss S, Bouza C, Krausch D et al.: Assessment of the safety and efficacy of the monoclonal anti-tumor necrosis factor antibody-fragment MAK 195F, in patients with sepsis and septic shock: a multicenter, randomized, placebo-controlled, dose-ranging study. Crit Care Med 1996, 24:733-742.
23. Abraham E, Glauser M, Butler T, Garbino J, Gelmon D, Laterre P, Kudsk K, Bruining HA, Otto C, Tobin E et al.: p55 tumor necrosis factor receptor fusion protein in the treatment of patients with severe sepsis and septic shock. J Am Med Assoc 1997, 277:1531-1538.
24. Marino M, Dunn A, Grail D, Inglese M, Noguchi Y, Richards E, Jungbluth A, Wada H, Moore M, Williamson B, Basu S, Old L: Characterization of tumor necrosis factor-deficient mice. Proc Natl Acad Sci USA 1997, 94:8093-8098. This paper includes the surprising observation that TNFα-/- mice are less able to resolve inflammation than wild type mice, suggesting an anti-inflammatory role of this cytokine.
25. Mueller R, Krahl T, Sarvetnick N: Pancreatic expresssion of interleukin-4 abrogates insulitis and autoimmune diabetes in nonobese diabetic (NOD) mice. J Exp Med 1996, 184:1093-1099.
26. Fox C, Danska J: IL-4 expression at the onset of islet inflammation predicts nondestructive insulitis in nonobese diabetic mice. J Immunol 1997, 158:2414-2424. This paper is an elegant study of the differences between the levels of various cytokines in NOD females and males during disease progression. It shows that increased IL-4 expression in the male during the early stages of disease correlates with protection from β cell destruction.
27. Teran LM, Davies DE: The chemokines: their potential role in allergic inflammation. Clin Exp Allergy 1996, 26:1005-1019.
28. Hulkower K, Brosnan CF, Aquino DA, Cammer W, Kulshretha S, Guida MP, Rapoport DA, Berman JW: Expression of CSF-1, c-fms, and MCP-1 in the central nervous system of rats with experimental allergic encephalomyelitis. J Immunol 1993, 150:2525-2533.
29. Ransohoff RM, Hamilton RA, Tani M, Stoler MH, Snick HE, Major JA, Estes ML, Thomas DM, Tuohy VK: Astrocyte expression of mRNA encoding cytokines IP-10 and JE/MCP-1 in experimental autoimmune encephalomyelitis. FASEB J 1993, 7:592-600.
30. Karpus WJ, Lukacs NW, McRae BL, Strieter RM, Kunkel SL, Miller SD: An important role for the chemokine macrophage inflammatory protein-1a in the pathogenesis of the T cell-mediated autoimmune disease, experimental autoimmune encephalomyelitis. J Immunol 1995, 155:5003-5010.
31. Grewal I, Rutledge B, Fiorillo J, Gu L, Gladue R, Flavell R, Rollins B: Transgenic monocyte chemoattractant protein-1 insulitis without diabetes. J Immunol 1997, 159:401-408. This paper demonstrates the in vivo activity of MCP-1 for monocytes and suggests that a chemotactic gradient is necessary for inflammatory cell recruitment. Using mice transgenic for MCP-1 under the control of the rat insulin promoter, the authors show recruitment of monocytes to the islets of Langerhans in the pancreas. Crossing these mice to a second transgenic animal that expresses MCP-1 under the control of an ubiquitously expressed MMTV promoter abrogates the monocytic infiltrate of the pancreas.
32. Fuentes M, Durham S, Swerdel M, Lewin A, Barton D, Megill J, Bravo R, Lira S: Controlled recruitment of monocytes and macrophages to specific organs through transgenic expression of monocyte chemoattractant protein-1. J Immunol 1995, 155:5769-5776.
33. Rutledge BJ, Rayburn H, Rosenberg R, North RJ, Gladue RP, Corless CL, Rollins BJ: High level monocyte chemoattractant protein-1 expression in transgenic mice increases their susceptibility to intracellular pathogens. J Immunol 1995, 155:4838-4843.
34. Gunn M, Nelken N, Lian X, Williams L: Monocyte chemoattractant protein-1 is sufficient for the chemotaxis of monocytes and lymphocytes in transgenic mice but requires an additional stimulus for inflammatory activation. J Immunol 1997, 158:376-383. This paper describes the only transgenic MCP-1 model in which T cells are recruited to the site of transgene expression. MCP-1 is expressed under the control of surfactant protein C promoter, and elevated numbers of both monocytes and T cells are recovered from the bronchoalveolar lavage fluid.
35. Lukacs N, Strieter R, Warmington K, Lincoln P, Chensue S, Kunkel S: Differential recruitment of leukocyte populations and alteration of airway hyperreactivity by C-C family chemokines in allergic airway inflammation. J Immunol 1997, 158:4398-4404.
36. Godiska R, Chantry D, Dietsch GN, Gray PW: Chemokine expression in murine experimental allergic encephalomyelitis. J Neuroimmunol 1995, 58:167-176.
37. Berman JW, Guida MP, Warren J, Amat J, Brosnan CF: Localization of monocyte chemoattractant peptide-1 expression in the central nervous system in experimental autoimmune encephalomyelitis and trauma in the rat. J Immunol 1996, 156:3017-3023.
38. Glabinski AR, Tani M, Strieter RM, Tuohy VK, Ransohoff RM: Synchronous synthesis of a- and b-chemokines by cells of diverse lineage in the central nervous system of mice with relapses of chronic experimental autoimmune encephalomyelitis. Am J Pathol 1997, 150:617-630.
39. Rot A, Krieger M, Brunner T, Bischoff SC, Schall TJ, Dahinden CA: RANTES and macrophage inflammatory protein 1a induce the migration and activation of normal human eosinophil granulocytes. J Exp Med 1992, 176:1489-1495.
40. Taub D, Turcovski-Corrales S, Key M, Longo D, Murphy W: Chemokines and T lymphocyte activation. J Immunol 1996, 156:2095-2103.
41. Karpus W, Lukacs N, Kennedy K, Smith W, Hurst S, Barrett T: Differential CC chemokine-induced enhancement of T helper cell cytokine production. J Immunol 1997, 158:4129-4136. This paper definitively demonstrates that chemokines can drive the differentiation of naive T cells into either Th1 or Th2 cells and influence the nature of cytokines that a T cell produces. MIP-1α or MCP-1 treatment of naive ovalbumin-specific T-cell receptor transgenic T cells caused differentiation of T cells into Th1 or Th2 cells respectively as measured by IFN-γ or IL-4 respectively.
42. Lukacs NW, Chensue SW, Karpus WJ, Lincoln P, Keefer C, Strieter RM, Kunkel SL: C-C chemokines differentially alter interleukin-4 production from lymphocytes. Am J Pathol 1997, 150:1861-1868.
43. Chensue SW, Warmington KS, Ruth JH, Sanghi PS, Lincoln P, Kunkel SL: Role of monocyte chemoattractant protein-1 (MCP-1) in Th1 (Mycobacterial) and Th2 (Schistosomal) antigen-induced granuloma formation. J Immunol 1996, 157:4602-4608.
44. De Togni P, Goellner J, Ruddle NH, Streeter PR, Fick A, Mariathasan S, Smith SC, Carlson R, Shornick LP, Strauss-Schoenberger J, Russell JH, Karr R, Chaplin DD: Abnormal development of peripheral lymphoid organs in mice deficient in lymphotoxin. Science 1994, 264:703-707.
45. Banks TA, Rouse BT, Kerley MK, Blair PJ, Godfrey VL, Kuklin NA, Bouley DM, Thomas J, Kanangat S, Mucenski ML: Lymphotoxin-alpha-deficient mice. Effects on secondary lymphoid organ development and humoral immune responsiveness. J Immunol 1995, 144:1685-1693.
46. Ryffel B, Di Padova F, Schreier MH, Le Hir M, Eugster HP, Quesniaux VF: Lack of type 2 T cell-independent B cell responses and defect in isotype switching in TNF-lymphotoxin alpha-deficient mice. J Immunol 1997, 158:2126-2133.
47. Matsumoto M, Mariathasan S, Nahm MH, Baranyay F, Peschon JJ, Chaplin DD: Role of lymphotoxin and the type I TNF receptor in the formation of germinal centers. Science 1996, 271:1289-1291. This paper shows that the splenic disorganization previously described in LTα-/- mice includes loss of germinal centers and reveals that p55TNFR1 -/- mice have some, but not all of the splenic defects of LTα-/- mice, indicating that germinal center formation involves multiple ligands and receptors in the LT/TNF family.
48. Koni PA, Sacca R, Lawton P, Browning JL, Ruddle NH, Flavell RA: Distinct roles in lymphoid organogenesis for lymphotoxins alpha and beta revealed in lymphotoxin beta-deficient mice. Immunity 1997, 6:491-500. The paper definitively shows that LTα's effects in lymphoid organ development are in part through its activities as an LTαβ complex, presumably through the LTβR, and in part as an LTα3 homotrimer through a new LTαR. The authors compare mice that are deficient in LTβ (LTβ-/- mice) developed in this paper by homologous recombination with LTα-/- mice developed previously (DeTogni et al., 1994 [44]). LTβ-/- mice have no PP, a disorganized spleen, and no peripheral LN, however, in contrast to LTα-/- mice, they do have mesenteric and cervical LN. These observations suggest that LTβ (presumably as an LTα1β2 complex) is crucial for the development of PP, splenic organization, and for peripheral LN, whereas LTα is sufficient for mesenteric and cervical LN, suggesting the existence of a novel LTαR.
49. H 186.2 gene.
50. •]) clearly indicate a role for p55TNFR1 in PP and germinal center development.
51. -/- mice have mesenteric and peripheral LN and develop PNA postitive bodies in the spleen after immunization, again confirming that LTα functions independently of LTβ in some aspects of LN and splenic development.
52. •] suggest that p55TNFR1's effect on PP is through LTα, not TNFα, and that full splenic organization involves LTα, LTαβ and TNFα. An inflammatory role for TNFα is suggested by the reduction but not the elimination of contact sensitivity.
53. -/- mice lack LN and PP and exhibit disorganized splenic white pulp. They show that mice deficient in p55TNFR1 lack organized PP, indicating that at least part of LT's role in PP development is through this receptor and most likely as LTα3.
54. Pfeffer K, Matsuyama T, Kunding TM, Wakeham A, Kishihara K, Shahinian A, Wiegmann K, Ohashi PS, Kronke M, Mak TW: Mice deficient for the 55kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succomb to L. monocytogenes infection. Cell 1993, 73:457-467.
55. Erickson SL, Sauvage FJD, Kikly K, Carver-Moore K, Pitts-Meek S, Gillett N, Sheehan KCF, Schreiber RD, Goeddel DV, Moore MW: Decreased sensitivity to tumour-necrosis factor but normal T-cell development in TNF receptor-2-deficient mice. Mature 1994, 372:560-563.
56. Forster R, Mattis AE, Kremmer E, Wolf E, Brem G, Lipp M: A putative chemokine receptor, BLR1, directs B cell migration to defined lymphoid organs and specific anatomic compartments of the spleen. Cell 1996, 87:1037-1047. This paper ties together chemokines and cytokines as inflammatory molecules and mediators of lymphoid organ development. In this paper, mice genetically deficient in BLR1, a protein with the characteristics of a chemokine receptor, lack inguinal LN, have very few or abnormal PP and exhibit abnormalities in splenic architecture. These data suggest that cytokines could effect lymphoid organ development, in part through the activation of chemokines that could attract cells to the developing organ.
57. Kratz A, Campos-Neto A, Hanson MS, Ruddle NH: Chronic inflammation caused by lymphotoxin is lymphoid neogenesis. J Exp Med 1996, 183:1461-1472. In this paper, the concept is proposed that inflammation can be considered to be a recapitulation of the events that occur in ontogeny with regard to lymphoid organ development. The authors suggest that the phenomenon of chronic inflammation be termed lymphoid neogenesis. This proposal derives from data obtained with mice that are transgenic for a construct consisting of the RIP driving expression of LTα. An analysis of the inflammation at the sites of transgene expression reveals that these sites have the characteristics of lymphoid organs with regard to cellular composition (T cells, B cells, dendritic cells and follicular dendritic cells), high endothelial venules, expression of mesenteric addressin and peripheral node addressin, and the ability to respond with antibody and undergo immunoglobulin class switching after immunization with an exogeneous antigen.
58. Chvatchko Y, Kosco-Vilbois M, Herren S, Lefort J, Bonnefoy J-Y: Germinal center formation and local immunoglobulin E (IgE) production in the lung after an airway antigenic challenge. J Exp Med 1996, 184:2353-2360.