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Infection and Immunity, March 2000, p. 1282-1288, Vol. 68, No. 3
Immunology and Disease Resistance Laboratory,
Livestock and Poultry Sciences Institute, Agricultural Research
Service, U. S. Department of Agriculture, Beltsville, Maryland
20705
Received 23 September 1999/Returned for modification 1 November
1999/Accepted 8 December 1999
The role of intestinal lymphocytes and gamma interferon (IFN-
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Eimeria tenella Infection Induces Local
Gamma Interferon Production and Intestinal Lymphocyte
Subpopulation Changes
)
production in protective immunity to Eimeria tenella
infection was evaluated in two inbred strains of chickens (SC and TK)
that display different patterns of susceptibility to coccidiosis. Oral inoculation of either strain with E. tenella led to
parasite invasion of the intestinal cecum and cecal tonsils. Greater
fecal oocyst shedding was seen in TK chickens. Flow cytometric analyses
of cecal tonsil lymphocytes demonstrated greater numbers of
CD4+ and T-cell receptor 
-positive
(TCR1+) cells in SC chickens and elevated numbers of
CD8+ and TCR2+ cells in TK chickens following
primary infection. IFN- mRNA expression was significantly increased
in cecal tonsil and intraepithelial lymphocytes at days 6 and 8, respectively, after primary infection in SC compared to TK chickens.
While no differences were noted between cecal tonsil lymphocytes of the
two strains following secondary infection, TK chickens showed elevated
IFN- transcript levels in intestinal intraepithelial lymphocytes at
this time. Selective depletion of CD4+, but not
CD8+, cecal tonsil lymphocytes in SC chickens resulted in a
reduced IFN- mRNA expression, indicating that CD4+ cells
are the primary source of this cytokine. Collectively, these results
indicate that local lymphocyte responses and production of IFN- are
influenced by host genetic factors.
*
Corresponding author. Mailing address: BARC-East,
Building 1040, IDRL, LPSI, USDA-ARS, Beltsville, MD 20705. Phone: (301) 504-8771. Fax: (301) 504-5306. E-mail:
hlilleho{at}lpsi.barc.usda.gov.
Present address: Laboratory of Molecular Biology, National Cancer
Institute, National Institutes of Health, Bethesda, MD 20892-4255.
Infection and Immunity, March 2000, p. 1282-1288, Vol. 68, No. 3
0019-9567/00/$04.00+0
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