NDLI: The Costimulatory Molecule ICOS Regulates Host Th1 and Follicular Th Cell Differentiation in Response to Plasmodium chabaudi chabaudi AS Infection.

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The Costimulatory Molecule ICOS Regulates Host Th1 and Follicular Th Cell Differentiation in Response to Plasmodium chabaudi chabaudi AS Infection.

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The Costimulatory Molecule ICOS Regulates Host Th1 and Follicular Th Cell Differentiation in Response to Plasmodium chabaudi chabaudi AS Infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wikenheiser, Daniel J. Stumhofer, Jason S. Ghosh, Debopam Kennedy, Brian
Description	Author Affiliation: Wikenheiser DJ ( Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205.); Ghosh D ( Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205.); Kennedy B ( Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205.); Stumhofer JS ( Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205 jstumhofer@uams.edu.)
Abstract	Blood-stage Plasmodium chabaudi chabaudi AS infection requires cell- and Ab-mediated immunity to control acute and persistent infection, respectively. ICOS regulates CD4(+) T cell activation and promotes the induction of follicular Th (TFH) cells, CD4(+) T cells that support B cell affinity maturation within germinal centers (GCs), resulting in the production of high-affinity Abs. In this article, we demonstrate that, in response to P. c. chabaudi AS infection, the absence of ICOS resulted in an enhanced Th1 immune response that reduced peak parasitemia. Despite the absence of ICOS, CD4(+) T cells were capable of expressing PD-1, B cell lymphoma 6, and CXCR5 during early infection, indicating TFH development was not impaired. However, by day 21 postinfection, Icos(-/-) mice accumulated fewer splenic TFHs compared with Icos(+/+) mice, leading to substantially fewer GC B cells and a decrease in affinity, but not production, of parasite-specific isotype-switched Abs. Moreover, treatment of mice with anti-ICOS ligand Abs to modulate ICOS-ICOS ligand signaling revealed a requirement for ICOS in TFH differentiation only after day 6 postinfection. Ultimately, the quality and quantity of isotype-switched Abs produced in Icos(-/-) mice declined over time, resulting in impaired control of persistent parasitemia. Collectively, these data suggest ICOS is not required for TFH induction during P. c. chabaudi AS infection or production of isotype-switched Abs, but it is necessary for maintenance of a sustained high-affinity, protective Ab response.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1403206
Journal	The Journal of Immunology
Issue Number	2
Volume Number	196
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2016-01-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Inducible T-cell Co-stimulator Protein Immunology Lymphocyte Activation Malaria T-lymphocyte Subsets T-lymphocytes, Helper-inducer Animals Cell Differentiation Disease Models, Animal Enzyme-linked Immunosorbent Assay Flow Cytometry Fluorescent Antibody Technique Germinal Center Cytology Mice Mice, Inbred C57bl Mice, Knockout Plasmodium Chabaudi Th1 Cells Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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