Webster H K, Wiesmann W P, Ward G S, Permpanich B, Pavia C S
Department of Immunology and Biochemistry, U.S. Army Medical Component, Armed Forces Institute for Medical Sciences, Bangkok, Thailand.
Immunopharmacology. 1990 May-Jun;19(3):169-75. doi: 10.1016/0162-3109(90)90066-n.
Peripheral blood lymphocytes were observed to have a defect in adenosine 3',5'-monophosphate (cAMP) metabolism during acute malaria infection which reversed once parasites were eliminated from the host circulation. The defect was characterized by decreased intracellular cAMP levels in lymphocytes and by hyporesponsiveness to adenosine or forskolin stimulation of cAMP production. These biochemical changes appeared to correlate functionally with a reduction in the proliferative response of lymphocytes to concanavalin A. A defect in the second messenger role of cAMP in immune effector cells may underlie immunosuppression in malaria infection.
在急性疟疾感染期间，外周血淋巴细胞被观察到在3',5'-环磷酸腺苷（cAMP）代谢方面存在缺陷，一旦寄生虫从宿主循环中清除，该缺陷就会逆转。该缺陷的特征是淋巴细胞内cAMP水平降低，以及对腺苷或福斯高林刺激产生cAMP的反应性降低。这些生化变化在功能上似乎与淋巴细胞对刀豆球蛋白A的增殖反应降低相关。cAMP在免疫效应细胞中的第二信使作用缺陷可能是疟疾感染中免疫抑制的基础。
