Interleukin-6 Deficiency Influences Cytokine Expression in Susceptible BALB Mice Infected with Leishmania major but Does Not Alter the Outcome of Disease
AUTOR(ES)
Titus, Richard G.
FONTE
American Society for Microbiology
RESUMO
Since interleukin-6 (IL-6) may promote Th2 responses, we infected BALB IL-6-deficient (IL-6−/−) mice with Leishmania major. There was not a significant difference between the courses of infection (lesion size and parasite burden) in IL-6−/− and wild-type mice, but IL-6−/− mice expressed lower levels of Th2- and Th1-associated cytokines.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=98619Documentos Relacionados
- Lack of Interleukin-6 (IL-6) Enhances Susceptibility to Infection but Does Not Alter Latency or Reactivation of Herpes Simplex Virus Type 1 in IL-6 Knockout Mice
- Suppression of interleukin-2 production by macrophages in genetically susceptible mice infected with Leishmania major.
- Complement Receptor 3 Deficiency Influences Lesion Progression during Leishmania major Infection in BALB/c Mice▿
- Myeloid Differentiation Antigen 88 Deficiency Impairs Pathogen Clearance but Does Not Alter Inflammation in Borrelia burgdorferi-Infected Mice
- Recombinant interleukin-1 alpha augments granuloma formation and cytokine production but not parasite clearance in mice infected with Leishmania donovani.