对硕大利什曼原虫LACK抗原产生反应的CD4(+) T细胞会迅速分泌白细胞介素-4，并且对具有抗性的B10.D2小鼠体内的宿主有害。
CD4(+) T cells which react to the Leishmania major LACK antigen rapidly secrete interleukin-4 and are detrimental to the host in resistant B10.D2 mice.
作者信息
Julia V, Glaichenhaus N
机构信息
Institut de Pharmacologie Moléculaire et Cellulaire, 06560 Valbonne, France.
出版信息
Infect Immun. 1999 Jul;67(7):3641-4. doi: 10.1128/IAI.67.7.3641-3644.1999.
Abstract
Leishmania major induces the rapid production of interleukin-4 (IL-4) in both susceptible BALB/c and resistant B10.D2 mice. In both strains, IL-4 is produced by T cells which react to the parasite LACK (for Leishmania homolog of the receptor for activated C kinase) antigen. The rapid production of IL-4 in B10.D2 mice does not confer susceptibility but results in increased parasite burdens.
摘要
硕大利什曼原虫可诱导易感的BALB/c小鼠和抗性的B10.D2小鼠快速产生白细胞介素-4（IL-4）。在这两种品系小鼠中，IL-4均由对寄生虫LACK（活化C激酶受体的利什曼原虫同源物）抗原产生反应的T细胞分泌。B10.D2小鼠中IL-4的快速产生并不会使其易感，但会导致寄生虫负荷增加。
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