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. Author manuscript; available in PMC: 2008 May 30.
Published in final edited form as: Curr Respir Med Rev. 2006 Aug;2(39):263–277. doi: 10.2174/157339806778019024

Table 5.

GASPID-Defective Mice

Genotype GASPID Deficiency Lung-Relevant Phenotype
C57Bl/6 mice Tryptase MCP7 Airway hyporesponsiveness; resistance to allergen sensitization
KitW/KitW-v or KitW-sh/KitW-sh Mast cell GASPIDs Lack of mast cells; decreased allergic inflammation; increased mortality from sepsis; enhanced bacterial bronchitis and pneumonia;
Ctsc −/− Activated chymases
Activated cathepsin G
Activated granzymes A & B
Activated tryptase MCP6
Decreased mortality from septic peritonitis;enhanced pneumonia
Gzma −/− Granzyme A Defective cell killinga
NE −/− Neutrophil elastase Protection from emphysemaa; defective bacterial killinga
Gzmm −/− Met-ase/Granzyme M Defective control of CMV infection
Gzmb −/− Granzyme B Defective cell killinga
Ctsg −/− Cathepsin G Defective neutrophil functiona
Mcpt1 −/− Chymase MCP1 Delayed parasite expulsion; delayed mast cell recruitment & structure
Mcpt4 −/− Chymase MCP4 Decreased activation of MMP gelatinases
Mcpt5 −/− Chymase/elastase MCP5(Carboxypeptidase A3) Resistance to ischemia-reperfusion injury
a

Many of these phenotypes are more dramatic when combined with other GASPID defects, as in Gzma (−/−) x Gzmb (−/−) or NE (−/−) x Ctsg (−/−) double-knockout strains (see text).