Reversal by lymphokines of the age-related hyporesponsiveness to contact sensitization and reduced Ia expression on Langerhans cells.
Reversal by lymphokines of the age-related hyporesponsiveness to contact sensitization and reduced Ia expression on Langerhans cells.
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淋巴因子逆转与年龄相关的接触致敏反应低下,并减少朗格汉斯细胞上的 Ia 表达。
DOI:
10.1007/bf00585926
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发表时间:
1987
影响因子:
3
通讯作者:
Baer,RL
中科院分区:
文献类型:
--
作者:
Belsito,DV;Dersarkissian,RM;Thorbecke,GJ;Baer,RL
Contact sensitivity responses were evaluated in young adult (3–5 months) and aged (16–26 months) BALB/c mice which were systemically treated with interleukin-2 (IL-2), interferon-γ (IFN-γ) or saline. Mice older than 16 months of age have deficient numbers of Ia+Langerhans cells in addition to their well-known impaired T cell functions. They also have an impaired cell-mediated response to contact sensitization with 1-chloro-2,4,6-trinitrobenzene. This hyporesponsiveness in aged mice can be almost completely reversed by ness in aged mice can be almost completely reversed by IL-2 and is marginally improved by IFN-γ. Exposure of skin from aged mice to interleukin-2 or interferon-γ, both in vivo and invvitro, causes increases in the density of Ia+Langerhans cells to levels approximating those in young mice. Since IFN-γ causes partial restitution while IL-2 fully restores the contact hypersensitivity in aged animals, we conclude that the hyporesponsiveness in aged mice results both from defective Ia antigen expression on the antigen-presenting Langerhans cells and from deficient T cell function.