TABLE 2.

Characteristics of E. vermifomis infections^a in mice with defects in cytokine production

Expt no.	Strain of mouseb	No. of mice	Primary infection		Secondary infection
			Oocyst output (106)	Patent period (days)	Oocyst output (106)	Patent period (days)
1	IFN-γ−/−	5	98.3 ± 14.8*	11.4 ± 0.7*	0.0 ± 0.0*	0.0 ± 0.0*
	C57 BL/6	5	16.4 ± 4.0†	8.2 ± 0.4†	0.0 ± 0.0*	0.0 ± 0.0*
	IFN-γ−/− primary controlc	5	ndd	nd	47.5 ± 4.6†	11.4 ± 0.4†
	C57 BL/6 primary control	5	nd	nd	10.8 ± 1.5‡	8.6 ± 0.2‡
2	IL-4−/−	7	13.2 ± 1.6*	8.0 ± 0.3*	0.0 ± 0.0*	0.0 ± 0.0*
	C57BL/6	8	12.5 ± 2.2*	7.9 ± 0.4*	0.0 ± 0.0*	0.0 ± 0.0*
	IL-4−/− primary control	6	nd	nd	9.4 ± 1.6†	8.2 ± 0.5†
	C57 BL/6 primary control	8	nd	nd	8.2 ± 0.9†	7.6 ± 0.3†
3	IL-6−/−	6	21.4 ± 1.5*	7.3 ± 0.3*	0.0 ± 0.0*	0.0 ± 0.0*
	IL-6+/+	6	8.8 ± 1.9†	7.0 ± 0.0*	0.0 ± 0.0*	0.0 ± 0.0*
	C57BL/6	6	10.2 ± 0.8†	7.2 ± 0.2*	0.0 ± 0.0*	0.0 ± 0.0*
	IL-6−/− primary control	6	nd	nd	16.9 ± 3.8†	7.7 ± 0.2†
	IL-6+/+ primary control	6	nd	nd	5.1 ± 1.2‡	7.0 ± 0.4‡
	C57 BL/6 primary control	6	nd	nd	7.6 ± 1.4‡	6.8 ± 0.2‡

^aAll infections were initiated with 10³ sporulated oocysts with secondary infections initiated 4 to 6 weeks after the primary infection. Oocyst outputs and patent periods are means, ± standard errors. Different symbols indicate significant differences in oocyst output or patent period (P < 0.05). 

^bMouse strain designations: −/−, homozygous targeted gene disruption; +/+, wild type. 

^cPrimary infection controls were naive mice infected in parallel with the secondary infections shown. 

^dnd, not done.