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Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
Published on: April 16, 2015
B cells express Ly-6C in a Th1 but not Th2 cytokine environment
Annette J Schlueter1, Arthur M Krieg, Peter De Vries
1Department of Pathology, University of Iowa College of Medicine, Iowa City, IA 52242-1181, USA. schluetera@uihc.uiowa.edu
Insights
Pro-inflammatory Th1 cytokines, especially Interferon-alpha (IFN-alpha), transiently induce Ly-6C expression on B cells. Th2 cytokines do not induce Ly-6C, and Ly6.1 mice show greater expression than Ly6.2 strains.
Area of Science:
- Immunology
- Cell Biology
Background:
- B cells typically do not express Ly-6C in a resting state.
- Ly-6C expression on B cells has been observed following exposure to pro-inflammatory stimuli.
- Understanding the regulation of Ly-6C expression on B cells is crucial for comprehending immune responses.
Purpose of the Study:
- To investigate the factors controlling Ly-6C expression on B cells.
- To determine the kinetics of Ly-6C expression in B cells under various conditions.
- To compare Ly-6C expression regulation between different mouse strains (Ly6.1 vs. Ly6.2).
Main Methods:
- In vivo studies using mouse models to assess cytokine effects on B cell Ly-6C expression.
- In vitro experiments exposing B cells to various cytokines (IFN-alpha, IFN-gamma, IL-4) and activators (anti-IgM, CD40 ligand).
- Comparative analysis of Ly-6C expression in Ly6.1 and Ly6.2 mouse strains.
Main Results:
- Pro-inflammatory Th1 cytokines, particularly Interferon-alpha (IFN-alpha) and Interferon-gamma (IFN-gamma), transiently upregulate Ly-6C expression on B cells.
- Polyclonal B cell activators showed limited independent induction but enhanced IFN-induced Ly-6C expression.
- Th2 cytokine environments, including Interleukin-4 (IL-4), did not induce Ly-6C expression and IL-4 antagonized IFN-driven induction.
- Ly6.1 mouse strains exhibited a greater capacity for B cell Ly-6C expression compared to Ly6.2 strains.
Conclusions:
- Th1, but not Th2, cytokine environments can transiently induce Ly-6C expression on B cells.
- IFN-alpha and IFN-gamma are key inducers of B cell Ly-6C expression.
- Significant differences exist in Ly-6C expression regulation between Ly6.1 and Ly6.2 mouse strains.
Abstract:
Interferon-alpha (IFN-alpha) is the primary regulator of transient Ly-6C expression on T cells. B cells, which do not express Ly-6C in the resting state, have been reported to express Ly-6C following exposure to proinflammatory stimuli. This study examined the factors controlling Ly-6C expression on B cells and the kinetics of Ly-6C expression in the presence of these factors. In vivo studies demonstrated that proinflammatory (Th1) cytokines transiently upregulate B cell Ly-6C expression. In vitro studies identified Th1 cytokines, particularly IFN-alpha and IFN-gamma, as the principal cytokines responsible for this induction. Polyclonal B cell activators (anti-IgM and recombinant CD40 ligand trimer) showed minimal ability to independently induce Ly-6C expression on B cells but did enhance the ability of IFNs to induce expression. Th2 cytokine environments did not result in B cell Ly-6C expression, and interleukin-4 (IL-4) actually antagonized the IFN-driven induction of Ly-6C. Ly6.1 strains of mice consistently demonstrated a greater ability to express Ly-6C on B cells than did Ly-6.2 strains. Together, these studies demonstrate the ability of Th1 but not Th2 cytokine environments to transiently induce the expression of Ly-6C on B cells and provide additional evidence for differences in the regulation of Ly-6C expression in Ly6.1 and Ly6.2 strains.
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