By Everard L. Napier, M.R.C.S., L.R.C.P. (Lond.). In charge Kala-azar research, Calcutta School of Tropical Medicine. Second edition. 185 pages of text with 15 charts in the text, 18 plates, and an appendix of references to literature, author index and subject index. Oxford University Press. London, Bombay, Calcutta, Madras, 1927
Centre for Medical Parasitology, Department of Infectious Diseases, University Hospital (Rigshospitalet) and Institute for Medical Microbiology and Immunology, University of Copenhagen, Malaria Administration, Department of Biochemistry, University of Khartoum, Department of Medical and Physiological Chemistry, University of Lund, Department of Microbiology, Brigham Young University, Copenhagen, Denmark
To explain the observation that acute Plasmodium falciparum malaria is associated with a transient inability of peripheral blood cells to respond to antigenic stimulation in vitro, we have postulated the disease-induced reallocation of peripheral lymphocytes, possibly by adhesion to inflamed endothelium. We measured plasma levels of soluble markers of endothelial inflammation and T cell activation in 32 patients suffering from acute, uncomplicated P. falciparum malaria, as well as in 10 healthy, aparasitemic control donors. All donors were residents of a malaria-endemic area of Eastern State Sudan. In addition, we measured the T cell surface expression of the interleukin-2 receptor (CD25) and the lymphocyte function-associated antigen (LFA-1; CD11a/CD18). We found that the plasma levels of all inflammation and activation markers were significantly increased in the malaria patients compared with the control donors. In addition, we found a disease-induced depletion of T cells with high expression of the LFA-1 antigen, particularly in the CD4+ subset. The results obtained provide further support for the hypothesis of T cell reallocation to inflamed endothelium in acute P. falciparum malaria.