Specific immunity to streptozocin. Cellular requirements for induction of lymphoproliferation

Diabetes ◽  
1988 ◽  
Vol 37 (1) ◽  
pp. 74-80 ◽  
Author(s):  
C. Klinkhammer ◽  
P. Popowa ◽  
H. Gleichmann
Keyword(s):  
2011 ◽  
Vol 35 (2) ◽  
pp. 256-261
Author(s):  
Wen-Xiang LI ◽  
Jun XIE ◽  
Rui SONG ◽  
Hong ZOU ◽  
Shan-Gong WU ◽  
...  

Immunology ◽  
2009 ◽  
Vol 128 (1pt2) ◽  
pp. e797-e804 ◽  
Author(s):  
Yu-Pei Liao ◽  
Chun-Chieh Wang ◽  
Dörthe Schaue ◽  
Keisuke S. Iwamoto ◽  
William H. McBride

Methods ◽  
1997 ◽  
Vol 12 (2) ◽  
pp. 155-164 ◽  
Author(s):  
Matthew F Mescher ◽  
Elena Savelieva

Parasitology ◽  
1984 ◽  
Vol 89 (3) ◽  
pp. 417-424 ◽  
Author(s):  
F. E. G. Cox ◽  
Stephanie M. Millott

SUMMARYMice pre-treated withCorynebacterium parvumand later challenged withPlasmodium vinckeibecome infected but do not die whereas control mice do. When pre-treated mice were challenged with 1, 10, 1 × 102, 1 × 104, 1 × 105or 1 × 106parasites, the pre-patent periods correlated directly with the number of parasites injected, but the subsequent parasitaemias reached similar levels. This suggests that parasite killing, resulting from pre-treatment withC. parvum, is not triggered until the parasite load has reached a particular threshold. The injection of alloxan monohydrate, which brings about the release of toxic oxygen inter mediates thought to be involved in non-specific immunity, has little effect onP. vinckeiinfections until the parasitaemia is relatively high. This indicates that oxygen-mediated parasite killing also does not occur until the parasitaemia has reached a particular threshold. It is suggested that it is only at relatively high parasitaemias that the factors involved in parasite killing are able to enter the infected red blood cells.


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