Am. J. Respir. Crit. Care Med.,
Volume 162, Number 4, October 2000, S161-S163
Cells and the Regulation of Mucosal
Immune Responses
ADRIAN C.
HAYDAY,
SCOTT
ROBERTS,
and
ELIZABETH
RAMSBURG
Peter Gorer Department of Immunobiology, Guy's, King's, and St. Thomas' Medical School, University of London, London, United Kingdom;
and Department of Molecular Cell and Developmental Biology and Section of Immunobiology, Yale University, New Haven, Connecticut
We are only now uncovering the potentially important contributions made to immune responses by 
cells. These contributions are likely to be particularly important at mucosal sites, where
cells are disproportionately enriched. Indeed, cells have proven
biological activity in the lung. In addition, cells are also enriched
in young rather than adult animals. Studies of mutant mice have
demonstrated that 
T cells are seemingly essential for high-affinity, cognate immunological memory, whereas cells contribute to
the early stages of an immune response and to the regulation of
T cell- and B cell-mediated immunity. To explore further the role of
cells in immune responses, we have investigated whether their
contribution is greater during the early period of life, when the cells
are more abundant. In a natural system of coccidial infection of gut
epithelial cells, we find that T cell responses are less essential for
immunoprotection during primary challenge of young mice than is
true for adult animals. This "ineffectiveness" creates a "window of
importance" for the immunoprotective capacity of cells, which
seem thereby to be more crucial in young compared with older animals. The relative ineffectiveness of T cells in young mice may be
attributable to a bias toward Th2 activity. We therefore hypothesize
that cell activity, elicited by infection early in life, may compensate for defects in Th1 activity and may actually accelerate the bias in T cells away from Th2. This has obvious implications for susceptibility to Th2-type allergic responses.
