Premium
Avian coccidiosis: changes in intestinal lymphocyte populations associated with the development of immunity to Eimeria maxima
Author(s) -
ROTHWELL LISA,
GRAMZINSKI ROBERT A.,
ROSE M. ELAINE,
KAISER PETER
Publication year - 1995
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1995.tb00883.x
Subject(s) - lamina propria , biology , cd8 , staining , epithelium , intestinal epithelium , immunology , intraepithelial lymphocyte , eimeria , lymphocyte , immune system , microfold cell , pathology , microbiology and biotechnology , medicine , genetics
Summary The effect of infection and subsequent challenge with Eimeria maxima on the populations of lymphocytes in the small intestine of Light Sussex chickens was assessed by immunohistochemistry. T cells were characterized for CD3, CD4, CD8, TCR1 (γδ heterodimer) or TCR2 (αβ 1 heterodimer) markers, and B cells for the expression of IgM, IgA andlgG. After a primary inoculum there were, in both the epithelium and the lamina propria, two distinct increases in the numbers of T lymphocytes. The first peaked on days 3–5 and the second, greater influx, on day 11 after infection. CD4+ and CD8+ cells were represented in both peaks but, whereas CD4+ cells were found almost exclusively in the lamina propria, CD8+ cells were present in both sites. The area staining positive for CD8+ cells was somewhat greater than the value obtained for CD4+ cells. In the epithelium there was an early, small increase in TCR1+‐staining, followed by a larger rise to the second peak, at which time there was also an increase in the lamina propria. Staining for TCR2+ cells followed the same pattern with a reversed distribution between epithelium and lamina propria. Changes after challenge were minimal and confined to the epithelium. The most notable changes in the expression of immunoglobulins were, in the lamina propria, a biphasic increase in the amount ofIgM+‐staining in the course of primary infection (corresponding approximately to that of the T cells), and in IgA + cells shortly after challenge.