Immune responses to T-dependent and T-independent antigens during visceral leishmaniasis in mice: evidence for altered T-cell regulation of immune responses to non-parasite antigens |
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| Authors: | S G Reed S B Roters J A Inverso T C Jones E A Goidl |
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| Institution: | 1. Cornell University Medical College, New York 10021 USA;2. The Federal University of Bahia, Salvador, Brazil;3. University of Maryland School of Medicine, Baltimore, Maryland 21201 USA;1. Departamento de Patologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil;2. Laboratório de Imunopatologia, CPqRR – FIOCRUZ, Belo Horizonte, Minas Gerais, Brazil;3. Department of Cell Biology and Molecular Genetics and Maryland Pathogen Research Institute and Center for Bioinformatics and Computational Biology, University of Maryland, College Park, MD, USA;1. Department of Pathological Sciences, Center of Biological Sciences, State University of Londrina, PR, Brazil;2. Universidade Alto Vale do Rio Peixe, Caçador, SC, Brazil;3. Department of Chemistry, Center of Exact Sciences, State University of Londrina, PR, Brazil;4. Department of Chemical Engineering and Food Engineering, Federal University of Santa Catarina, SC, Brazil;1. Department of Zoonoses, Faculty of Veterinary Medicine, Sohag University, Sohag 82524, Egypt;2. Biology Department, College of Science, Jouf University, Sakaka, Aljouf 2014, Saudi Arabia;3. Department of Medical Parasitology, Faculty of Medicine, Zagazig University, Zgazig, Egypt |
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| Abstract: | Antibody responses to T-dependent and T-"independent" antigens were studied in disease-susceptible (BALB/c and C57BL/10) and disease-resistant (A/J) mice infected with Leishmania donovani chagasi. Disease-susceptible mice but not disease-resistant mice showed a transient decrease in PFC responses to TNP on a T-dependent carrier (BGG) during the period of 4-8 weeks after infection. Infected disease-susceptible animals also showed increased responses to TNP on a type II T-independent carrier (Ficoll), which persisted until at least 14 weeks after infection. The increased responses were associated with a significant increase in anti-TNP antibody of the IgG2b subclass. When T-enriched spleen cells from infected mice and B-enriched spleen cells from uninfected mice were transferred to irradiated recipients immunized with TNP-Ficoll, increased anti-TNP PFC were observed over numbers seen in irradiated recipients which received both B and T cells from uninfected mice. Increased responses to TNP-Ficoll were also induced by prior administration of soluble leishmania extract in CFA. Infected mice immunized with TNP-LPS, a T-independent type I antigen, also had increased anti-TNP antibody responses, but had normal anti-LPS antibody responses. The elevated antibody production which occurred in response to the T-"independent" antigens could not be attributed to the relatively low polyclonal response which occurred in both disease-resistant and disease-susceptible mice infected with L. donovani chagasi. The observations are consistent with leishmania induced, transient alterations in some T-cell functions including response to haptens on T-dependent carriers, and a lack of down regulation of T-"independent" responses. Subtle lesions in immunoregulation may be important correlates of successful protozoal infection and may be responsible for some of the immunologic manifestations of the disease. |
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