Absence of Follicular Dendritic Cells (FDC) in Mutant Mice with Deficient TNF/Lymphotoxin (LT) Signaling

M, Le Hir; Hp, Eugster

doi:10.1007/978-1-4757-9966-8_80

Advances in Experimental Medicine and Biology

1997

DOI: 10.1007/978-1-4757-9966-8_80

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Absence of Follicular Dendritic Cells (FDC) in Mutant Mice with Deficient TNF/Lymphotoxin (LT) Signaling

Le Hir M

Eugster Hp

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Cited by 3 publications

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Two waves of memory B-cell generation in the primary immune response

Inamine¹,

Takahashi²,

Baba³

et al. 2005

International Immunology

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Memory B cells can be generated independently of germinal center (GC) formation and affinity maturation in Bcl-6-deficient mice, but the contribution of the GC-independent pathway for memory B-cell generation in normal mice remains unknown. To examine this, we administrated anti-inducible co-stimulator (ICOS) mAbs into mice at the onset of GC formation in the primary response. This manipulation affected the generation of GC B cells in the spleen, but neither IgG1 memory B cell nor production of IgG1 long-term antibody was affected. In ICOS-manipulated mice, GC B cells accumulated somatic mutations in the IgV(H) genes and underwent affinity maturation; however, memory B cells scarcely accumulated mutations and reconstituted the secondary response by low affinity, supporting the notion that low-affinity memory B cells are generated in a GC-independent manner. Thus, it appears that memory B cells are established by two different pathways, associated with or without GC reaction and affinity maturation. The generation and long-term persistence of low-affinity IgG1 memory B cells and antibodies in ICOS-manipulated mice support the idea that low-affinity memory B cells may give rise to long-term antibody-forming cells.

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Two waves of memory B-cell generation in the primary immune response

Inamine¹,

Takahashi²,

Baba³

et al. 2005

International Immunology

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Dismantling the Germinal Center: Comparing the Processes of Transformation, Regression, and Fragmentation of the Lymphoid Follicle

Jones¹

2002

Advances in Anatomic Pathology

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The pathologic and immunologic features of the formation of the germinal center have been extensively studied. The process of dissolution of the germinal center is not as well understood. Different patterns of germinal-center breakdown are commonly encountered in diagnostic lymph node biopsy specimens and frequently present difficulties in diagnosis. The current immunologic understanding of germinal-center dynamics is reviewed and correlated with the histologic and immunophenotypic features of three broad classes of germinal center dissolution, namely progressive transformation, regression, and follicle fragmentation. The author suggests that these different patterns represent alternate responses to antigenic stimulation. The relationships of progressive transformation to Hodgkin's disease and of follicular regression to Castleman's disease are discussed.

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Differential T Cell-Mediated Regulation of CD23 (FcεRII) in B Cells and Follicular Dendritic Cells

Sukumar

Conrad

Szakal

et al. 2006

The Journal of Immunology

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Differences in murine follicular dendritic cells (FDC)-CD23 expression under Th1 vs Th2 conditions prompted the hypothesis that T cells help regulate the phenotype of FDCs. FDCs express CD40, suggesting that T cell-CD40L and lymphokines may be involved in regulating FDC-CD23. To test this, highly enriched FDCs were incubated with CD40L trimer or anti-CD40 to mimic T cell signaling in the presence of IFN-γ or IL-4. Surface expression of CD23 was determined by flow cytometry, whereas mRNA levels of CD23 and its isoforms CD23a and CD23b were independently measured by quantitative PCR. When FDCs were incubated with either CD40L trimer or agonistic anti-CD40 Ab, the expression of FDC-CD23 was increased both at the mRNA and protein levels. Moreover, engagement of FDC-CD40 enhanced mRNA levels for both CD23a and CD23b isoforms. In addition, IFN-γ substantially enhanced CD23a and CD23b mRNA levels in CD40-stimulated FDCs. Curiously, IL-4 could also up-regulate FDC-CD23a but not -CD23b. Anti-IFN-γ dramatically inhibited FDC-CD23 in mice immunized with CFA, whereas anti-IL-4 had only a modest inhibitory effect. In contrast with FDCs, IFN-γ inhibited surface expression of murine B cell-CD23 as well as mRNA for B cell CD23a and -CD23b, whereas IL-4 dramatically enhanced message for both isoforms as well as protein expression. In short, CD23 was regulated very differently in FDCs and B cells. Previous studies suggest that high levels of FDC-CD23 inhibit IgE production, and this IFN-γ and CD40L-mediated up-regulation of FDC-CD23 may explain, at least in part, why Th1 responses are associated with low IgE responses in vivo.

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Absence of Follicular Dendritic Cells (FDC) in Mutant Mice with Deficient TNF/Lymphotoxin (LT) Signaling

Cited by 3 publications

References 20 publications

Two waves of memory B-cell generation in the primary immune response

Two waves of memory B-cell generation in the primary immune response

Dismantling the Germinal Center: Comparing the Processes of Transformation, Regression, and Fragmentation of the Lymphoid Follicle

Differential T Cell-Mediated Regulation of CD23 (FcεRII) in B Cells and Follicular Dendritic Cells

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