NDLI: Acute Plasmodium chabaudi infection dampens humoral responses to a secondary T-dependent antigen but enhances responses to a secondary T-independent antigen.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wilmore, Joel R. Maue, Alexander C. Lefebvre, Julie S. Rochford, Rosemary Haynes, Laura
Description	Author Affiliation: Wilmore JR ( Department of Microbiology and Immunology, State University of New York, Upstate Medical University, Syracuse, NY 13210)
Abstract	High rates of coinfection occur in malaria endemic regions, leading to more severe disease outcomes. Understanding how coinfecting pathogens influence the immune system is important in the development of treatment strategies that reduce morbidity and mortality. Using the Plasmodium chabaudi mouse model of malaria and immunization with model Ags that are either T-dependent (4-hydroxy-3-nitrophenyl [NP]-OVA) or T-independent (NP-Ficoll), we analyzed the effects of acute malaria on the development of humoral immunity to secondary Ags. Total Ig and IgG1 NP-specific Ab responses to NP-OVA were significantly decreased in the P. chabaudi-infected group compared with the uninfected group, whereas NP-specific IgG2c Ab was significantly increased in the P. chabaudi-infected group. In contrast, following injection with T-independent NP-Ficoll, the P. chabaudi-infected group had significantly increased NP-specific total Ig, IgM, and IgG2c Ab titers compared with controls. Treatment with anti-IFN-Î³ led to an abrogation of the NP-specific IgG2c Ab induced by P. chabaudi infection but did not affect other NP-specific Ab isotypes or titers. IFN-Î³ depletion also increased the percentage of plasma cells in both P. chabaudi-infected and uninfected groups but decreased the percentage of B cells with a germinal center (GC) phenotype. Using immunofluorescent microscopy, we were able to detect NP(+) GCs in the spleens of noninfected mice, but there were no detectible NP(+) GCs in mice infected with P. chabaudi. These data suggest that during P. chabaudi infection, there is a shift toward an extrafollicular Ab response that could be responsible for decreased Ab responses to secondary T-dependent Ags.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	9
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antibodies, Protozoan Blood Antigens, Protozoan Immunology Antigens, T-independent Malaria Plasmodium Chabaudi Animals Antibody Formation Disease Models, Animal Ficoll Germinal Center Immunoglobulin G Immunoglobulin M Interferon-gamma Mice Mice, Inbred C57bl Ovalbumin T-lymphocytes Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Research Support, U.s. Gov't, Non-p.h.s. Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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