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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Communicable Disease Control

 
 
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Disease relevance of Communicable Disease Control

 

High impact information on Communicable Disease Control

  • Susceptible BALB/c mice aberrantly develop Th2 cells in response to infection and are unable to control parasite dissemination [6].
  • Mice that produced low amounts of MSP1-15 stimulated IFN-gamma and could not control parasite infection [7].
  • Finally, IL-12 is required to sustain Th1 cells and control parasite growth in susceptible and resistant strains of mice during primary and secondary infection [8].
  • Although Stat1-/- mice produced normal serum levels of IL-12 and IFN-gamma, these mice were unable to control parasite replication and rapidly succumbed to this infection [9].
  • Here we report that mice lacking the p75 receptor (TNFRp75-/-) or both receptors (TNFRp55p75-/-), also control parasite replication, albeit mice lacking the p55 receptor (either TNFRp55-/- or TNFRp55p75-/-) are delayed in their elimination of L. major compared with controls [10].
 

Biological context of Communicable Disease Control

 

Anatomical context of Communicable Disease Control

 

Associations of Communicable Disease Control with chemical compounds

 

Gene context of Communicable Disease Control

  • These results suggest that, in male mice, a rapid response to infection with high levels of TNF-alpha and IFN-gamma helps to control parasite multiplication, after which IL-10 production may be important in down regulating these potentially harmful inflammatory mediators [24].
  • Nevertheless, in both the acute and chronic stages, IFN-gamma-dependent but iNOS-independent mechanism(s) play a major function in parasite control and their identification remains an important challenge for this field [25].
  • CCL5 is part of the cascade of events leading to efficient parasite control in L. major infection [26].
  • Our data indicate that endothelin ET(A) receptors contribute to the initial mechanisms of parasite control [27].
  • The signal was present in the draining popliteal lymph nodes of both hosts, however, only susceptible mice known to be unable to control parasite dissemination showed induction of HDC in their distant periaortic lymph nodes as well [28].

References

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