Visceral Leishmaniasis in mice devoid of tumor necrosis factor and response to treatment

Infection and Immunity

Volumn 68, Issue 11, 2000, Pages 6289-6293

  Murray, H W ^a   Jungbluth, A ^a   Ritter, E ^a   Montelibano, C ^a   Marino, M W ^a  

^a Box 136 ^*  (United States)

Author keywords

[No Author keywords available]

Indexed keywords

AMPHOTERICIN B; ANTIMONY; MILTEFOSINE; TUMOR NECROSIS FACTOR;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CHEMOTHERAPY; CONTROLLED STUDY; HEPATITIS; KNOCKOUT MOUSE; LEISHMANIA DONOVANI; LIVER GRANULOMA; LIVER NECROSIS; MORTALITY; MOUSE; NONHUMAN; PRIORITY JOURNAL; SURVIVAL; VISCERAL LEISHMANIASIS;

AMPHOTERICIN B; ANIMAL; FEMALE; LEISHMANIA DONOVANI; LEISHMANIASIS, VISCERAL; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; SUPPORT, U.S. GOV'T, P.H.S.; TH1 CELLS; TUMOR NECROSIS FACTOR;

EID: 0033785362     PISSN: 00199567     EISSN: None     Source Type: Journal    
DOI: 10.1128/IAI.68.11.6289-6293.2000     Document Type: Article

References (37)

1. Structural deficiencies in granuloma formation in TNF gene-targeted mice underlie the heightened susceptibility to aerosol Mycobacterium tuberculosis infection, which is not compensated for by lymphotoxin
2. Tumor necrosis factor in the pathogenesis of infectious diseases
3. IL-10 production is enhanced in human T cells by IL-12 and IL-6 and in monocytes by tumor necrosis factor-α
4. Crucial role of TNF receptor type 1 (p55), but not of TNF receptor type 2 (p75) in murine toxoplasmosis
5. Induction by IL-1 and interferon-γ: Tissue distribution, biochemistry, and function of a natural adherence molecule (ICAM-1)
6. Fatal granuloma necrosis without exacerbated mycobacterial growth in tumor necrosis factor receptor p55 gene-deficient mice intravenously infected with Mycobacterium avium
7. Tumor necrosis factor-α is required in the protective immune response against Mycobacterium tuberculosis in mice
8. Inhibition of interferon gamma induced interleukin 12 production: A potential mechanism for the anti-inflammatory activities of tumor necrosis factor
9. TNF receptor p55 is required for elimination of inflammatory cells following control of intracellular pathogens
10. Strategies for immune intervention in visceral leishmaniasis
11. Tumor necrosis factor-α synergizes with IFN-γ in mediating killing of Leishmania major through the induction of nitric oxide
12. Characterization of tumor necrosis factor-deficient mice
13. Granulomatous inflammation: Host antimicrobial defense in the tissues in visceral leishmaniasis
14. Endogenous interleukin-12 regulates acquired resistance in experimental visceral leishmaniasis
15. Visceral leishmanicidal activity of hexadecylphosphocholine (miltefosine) in mice deficient in T cells and activated macrophage microbicidal mechanisms
16. Roles of endogenous gamma interferon and macrophage microbicidal mechanisms in host response to chemotherapy in experimental visceral leishmaniasis
17. Treatment of experimental visceral leishmaniasis in a T-cell-deficient host: Response to amphotericin B and pentamidine
18. Models of relapse of experimental visceral leishmaniasis
19. Macrophage microbicidal mechanisms in vivo: Reactive nitrogen versus oxygen intermediates in the killing of intracellular visceral Leishmania donovani
20. Successful response to chemotherapy in experimental visceral leishmaniasis: Requirement for T cells and effect of lymphokines
21. Control of Leishmania major infection in mice lacking TNF receptors
22. Activated T cells induce macrophages to produce NO and control Leishmania major in the absence of tumor necrosis factor receptor p55
23. Enhanced sensitivity of tumor necrosis factor/lymphotoxin-α-deficient mice to Cryptococcus neoformans infection despite increased levels of nitrite/nitrate, interferon-γ and interleukin-12
24. Modification of in vitro monocyte cytokine responses to Leishmania donovani: Interferon-γ prevents parasite-induced inhibition of interleukin-1 production and primes monocytes to respond to Leishmania by producing both tumor necrosis factor-α and interleukin-1
25. Role of inorganic nitrogen oxides and tumor necrosis factor alpha in killing Leishmania donovani amastigotes in gamma interferon-lipopolysaccharide-activated macrophages from Lsh(s) and Lsh(r) congenic mouse strains
26. Mice lacking the tumour necrosis factor receptor 1 are resistant to TNF-mediated toxicity but highly susceptible to infection by Listeria monocytogenes
27. Costimulation by purified intracellular adhesion molecule 1 and lymphocyte function-associated antigen 3 induces distinct proliferation, cytokine and cell surface antigen profiles in human 'naive' and 'memory' CD4+ cells
28. Cytokine interactions in experimental cutaneous leishmaniasis. II. Endogenous tumor necrosis factor-α production by macrophages is induced by synergistic action of interferon (IFN)-γ and interleukin (IL) 4 and accounts for the antiparasitic effect mediated by IFN-γ and IL 4
29. Trial of oral miltefosine for visceral leishmaniasis
30. Immunomodulatory and immunotherapeutic properties of recombinant interferon-γ and recombinant tumor necrosis factor in mice
31. Intracellular antimicrobial activity in the absence of interferon-γ: Effect of interleukin-12 in experimental visceral leishmaniasis in interferon-γ gene-disrupted mice
32. Augmentation of murine tumor necrosis factor production by amphotericin B in vitro and in vivo
33. Role and effect of TNF-α in experimental visceral leishmaniasis
34. The pathophysiology of tumor necrosis factors
35. Mice lacking the TNF receptor p55 fail to resolve lesions caused by infection with Leishmania major, but control parasite replication
36. Decreased resistance of TNF receptor p55- and p75-deficient mice to chronic toxoplasmosis despite normal activation of inducible nitric oxide synthase in vivo
37. Influence of hexadecylphosphocholine on the release of tumor necrosis factor and nitroxide from peritoneal macrophages in vitro