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T Regulatory Cell Levels Decrease in People Infected With Schistosoma mansoni on Effective Treatment

Schistosomiasis mansoni is usually a chronic infection that leads to long-term, systemic exposure to schistosome antigens. Experimental Schistosoma mansoni infection is associated with immunoregulatory mechanisms, including T regulatory cells (Treg) that may help control morbidity and dampen resistance to re-infection. We now show that some schistosomiasis mansoni patients have high proportions of CD3⁺/CD4⁺/CD25^high Treg. On effective treatment with praziquantel, these high Treg percentages decrease, and fewer of the remaining Treg express CD45RO. The proportion of Treg in S. mansoni–infected patients is inversely related to their percentage of activated, putative effector T cells (CD3⁺/CD4⁺/CD25^medium/HLA-DR⁺ cells). We conclude some, but not all, schistosomiasis mansoni patients develop high percentages of circulating Treg, and effective treatment both decreases the levels of these cells and changes their phenotypes, possibly because of the removal of constant exposure to antigens from intravascular, egg-producing adult worms.

Received April 27, 2007. Accepted for publication June 25, 2007.

Acknowledgments: The authors thank Eric Livaha and all other technical and field staff of the Schistosomiasis Immunology Laboratory (KEMRI) for their professional assistance. This paper is published with the permission of the Director of the Kenya Medical Research Institute. The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the Centers for Disease Control and Prevention.

Financial support: KW was supported in part by the Japan Health Sciences Foundation, CLB was supported by Public Health Service (PHS) Grant T32 AI 060546 from the National Center for Allergy and Infectious Diseases (NIAID) of the National Institutes of Health (NIH) and a training grant from the Ellison Medical Foundation, PNMW was supported by PHS Grant D43 TW007123 from the Fog-arty International Center, NIH, and the studies were supported by PHS Grant AI 053695 from the NIAID of the National Institutes of Health, the PHS, Centers for Disease Control and Prevention, and the Kenya Medical Research Institute.

^* Address correspondence to Daniel G. Colley, Center for Tropical and Emerging Global Diseases, Coverdell Center, Room 145, University of Georgia, 500 D.W. Brooks Drive, Athens, GA 30602-3799. E-mail: dcolley{at}uga.edu

Authors’ addresses: Kanji Watanabe, Institute of Tropical Medicine, Nagasaki University (NEKKEN), 1-12-4 Sakamoto, Nagasaki 852-8523, Japan, E-mail: watakanj{at}net.nagasaki-u.ac.jp. Pauline N.M. Mwinzi, Diana M.S. Karanja, and Erick M.O. Muok, Vector Biology and Control Research Centre, Kenya Medical Research Institute, PO Box 1578, Kisumu, Kenya, E-mails: pmwinzi{at}kisian.mimcom.net, dkaranja{at}kisian.mimcom.net, and emouk{at}kisian.mimcom.net. Carla L. Black and Daniel G. Colley, Center for Tropical and Emerging Global Diseases, Room 145 Coverdell Center, University of Georgia, Athens, GA 30602-7399, E-mails: blackc{at}uga.edu and dcolley{at}uga.edu. W. Evan Secor, Division of Parasitic Diseases, Centers for Disease Control and Prevention, 4770 Buford Highway, N.E., Mail-stop F-13, Atlanta, GA 30341, E-mail: was4{at}cdc.gov.

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