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pubmed:abstractText |
Between weaning (3 wk of age) and adulthood (7 wk of age), mice develop increased resistance to infection with Eimeria vermiformis, an abundant intestinal parasite that causes coccidiosis. This development of resistance was perturbed in T cell receptor (TCR)delta(-/-) mice, which at 4 wk of age remained largely susceptible to infection and prone to infection-associated dehydration. These phenotypes were rescued by the repopulation of gammadelta cells after adoptive transfer of lymphoid progenitors into newborn recipients. Because alphabeta T cells are necessary and sufficient for the protection of adult mice against E. vermiformis, the requirement for gammadelta cells in young mice shows a qualitative difference between the cellular immune responses operating at different ages. An important contribution toward primary immune protection in young hosts may have provided a strong selective pressure for the evolutionary conservation of gammadelta cells. This notwithstanding, the development of effective, pathogen-specific immunity in young mice requires alphabeta T cells, just as it does in adult mice.
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