Reversible defect in cAMP metabolism in lymphocytes in malaria infection.
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.
Webster
H K
HK
Department of Immunology and Biochemistry, U.S. Army Medical Component, Armed Forces Institute for Medical Sciences, Bangkok, Thailand.
Wiesmann
W P
WP
Ward
G S
GS
Permpanich
B
B
Pavia
C S
CS
D015087:2',3'-Cyclic-Nucleotide Phosphodiesterases / Q000097:blood; D000241:Adenosine / Q000494:pharmacology; D000818:Animals; D005576:Colforsin / Q000494:pharmacology; D003208:Concanavalin A / Q000494:pharmacology; D000242:Cyclic AMP / Q000097:blood*; D007108:Immune Tolerance; D066298:In Vitro Techniques; D008213:Lymphocyte Activation; D008214:Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D008253:Macaca mulatta; D008288:Malaria / Q000097:blood* / Q000276:immunology; D008297:Male
D003208:Concanavalin A; D005576:Colforsin; D000242:Cyclic AMP; D015087:2',3'-Cyclic-Nucleotide Phosphodiesterases; D000241:Adenosine