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Diminished in vitro production of interleukin-1 and tumor necrosis factor-alpha during acute visceral leishmaniasis and recovery after therapy.
- Source :
-
The Journal of infectious diseases [J Infect Dis] 1992 Jun; Vol. 165 (6), pp. 1094-102. - Publication Year :
- 1992
-
Abstract
- Disturbance of T cell-mediated immunity has been reported in acute visceral leishmaniasis (AVL). In a study of 16 patients with AVL, defective production of interleukin-1 (IL-1) by peripheral blood mononuclear cells was demonstrated in response to leishmania antigens, heat-killed Listeria organisms, and lipopolysaccharide when compared to posttherapy values or controls. This global defect in IL-1 production was corrected after successful therapy. Twelve of 16 patients responded with a greater than or equal to 2.5-fold increase in IL-1 production that correlated with clinical cure, P less than .01. Depressed production of tumor necrosis factor (TNF) was leishmania antigen-specific and similarly recovered after therapy. In vitro TNF production during the follow-up period did not correlate with clinical status but high serum levels were associated with AVL. Since T cells are activated by processed antigens presented on class II major histocompatibility molecules and by newly synthesized IL-1, defective IL-1 production may contribute to the immunosuppression observed in AVL.
- Subjects :
- Acute Disease
Adolescent
Adult
Cells, Cultured
Child
Child, Preschool
Dose-Response Relationship, Immunologic
Humans
Immune Sera immunology
Leishmaniasis, Visceral therapy
Lipopolysaccharides immunology
Listeria monocytogenes immunology
Treatment Outcome
Interleukin-1 biosynthesis
Leishmaniasis, Visceral immunology
Leukocytes, Mononuclear immunology
Tumor Necrosis Factor-alpha biosynthesis
Subjects
Details
- Language :
- English
- ISSN :
- 0022-1899
- Volume :
- 165
- Issue :
- 6
- Database :
- MEDLINE
- Journal :
- The Journal of infectious diseases
- Publication Type :
- Academic Journal
- Accession number :
- 1583328
- Full Text :
- https://doi.org/10.1093/infdis/165.6.1094