CD4 T cell priming in dendritic cell-deficient mice

Castiglioni, Paola; Lu, Christina; Lo, David; Croft, Michael; Langlade‐Demoyen, Pierre; Zanetti, Maurizio; Gerloni, Mara

doi:10.1093/intimm/dxg015

Cited by 18 publications

(17 citation statements)

References 40 publications

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“…We found that Tg B lymphocytes failed to directly activate OVAspecific TCR-transgenic CD8 T cells (Fig. 3B), a result at variance with our previous report that OVA-specific TCR-transgenic CD8 T cells are readily activated by DC pulsed with OVA [21]. …”

Section: Differential Activation Of Cd4 and Cd8 T Cells By Antigen-prcontrasting

confidence: 98%

CD8 T cell priming by B lymphocytes is CD4 help dependent

Castiglioni¹,

Gerloni²,

Cortez-Gonzalez³

et al. 2005

Eur J Immunol

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While it is generally accepted that B lymphocytes can present antigen and activate CD4 T cells, priming of CD8 T cells by B lymphocytes remains controversial. Recently, we showed that mice injected with genetically programmed B lymphocytes generate antigen specific CD4 and CD8 T cell responses in vivo that could also be induced in mice lacking functional dendritic cells. To gain further insights into the requirements for T cell priming by antigen-presenting B lymphocytes, in vitro experiments were performed using ovalbumin (OVA) and OVA-specific TCR-transgenic CD4 and CD8 T cells. We found that while B lymphocytes can directly prime CD4 T cells, the activation of CD8 T cells requires T cell help. Transfer experiments show that help can either be contact dependent or be mediated by soluble factors in the supernatants of activated OVAspecific CD4 T cells. Furthermore, the effect of activated CD4 T cells can be replaced by soluble recombinant IL-4. Collectively, the data show the existence of different requirements for priming of CD4 and CD8 T cells and point to the previously unappreciated fact that the induction of CD8 T cell responses by B lymphocytes requires T cell help.

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Section: Differential Activation Of Cd4 and Cd8 T Cells By Antigen-prcontrasting

confidence: 98%

CD8 T cell priming by B lymphocytes is CD4 help dependent

Castiglioni¹,

Gerloni²,

Cortez-Gonzalez³

et al. 2005

Eur J Immunol

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“…3). In agreement with data published elsewhere [22] the CD4 T cell response in relB -/-BM chimeras was also comparable to that measured in control C57BL/6 BM chimeras (stimulation index 7.6±0.8 vs. 9.8±2). These results suggest that CTL priming in the spleen in the model of somatic transgene immunization may occur in the absence of functional BM-derived DC.…”

Section: Ctl Priming In Vivo In Dc-deficient Micesupporting

confidence: 92%

“…However, because CTL priming was possible in relB -/-BM chimeras, whose spleen DC are unable to prime T cell responses to soluble antigen in vitro and in vivo [22], we argue that DC are dispensable in T cell priming in this model. Cross-priming can be ruled out on the basis of two additional considerations.…”

Section: Discussionmentioning

confidence: 83%

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Role of T cell help and endoplasmic reticulum targeting in protective CTL response against influenza virus

et al. 2003

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We report on the induction of primary and long-term memory cytotoxic T lymphocyte (CTL) responses against the nucleoprotein of the influenza virus A/PR8/34 in mice immunized with plasmid DNA targeted to B lymphocytes in the spleen. We found that the magnitude of the CTL response and the size of the pool of memory CTL was greater when the CTL response was induced in presence of T cell help. Interestingly, immunization with a signal sequencecompetent transgene was markedly superior to immunization with a transgene lacking the endoplasmic reticulum (ER) targeting sequence, in inducing CTL. We also found a correlation between in vivo protection from lethal virus challenge and (1) the availability of T cell help and (2) ER targeting. Immunization of dendritic cell-deficient mice suggests that B lymphocytes function as antigen-presenting cells in this model of immunization. Collectively, the results suggest that somatic transgene immunization is a conceptually new approach to induce effective anti-viral CTL responses and to assess the parameters critical for long-lasting and protective CTL responses in vivo.

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“…In relB Ϫ/Ϫ mice, deficient in myeloid and functional lymphoid DCs, CD4 ϩ T cells can be primed in response to soluble protein Ag, suggesting that B cells play a role in T cell priming in the absence of DC functions (54). In mice lacking B cells, primary CD4 ϩ or CD8 ϩ T cell priming can be generated (55).…”

Section: Discussionmentioning

confidence: 99%

Marginal Zone, but Not Follicular B Cells, Are Potent Activators of Naive CD4 T Cells

Attanavanich

Kearney

2004

The Journal of Immunology

236

210

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The early involvement of marginal zone (MZ) B lymphocytes in T-independent immune responses is well established. In this study we compared the abilities of MZ and follicular (FO) B cells to collaborate with T cells. After immunization with soluble hen egg lysozyme, both MZ and FO B cells captured Ag and migrated to T cell areas in the response to hen egg lysozyme. MZ B cells were far superior to FO B cells in inducing CD4+ T cell expansion both in vitro and in vivo. MZ, but not FO, B cells, after interaction with T cells, differentiated into plasma cells, and in addition they stimulated Ag-specific CD4+ T cells to produce high levels of Th1-like cytokines upon primary stimulation in vitro. These results indicate that MZ B cells rapidly and effectively capture soluble Ag and activate CD4+ T cells to become effector T cells. The enhanced capacity of MZ B cells to prime T cells in this study appeared to be intrinsic to MZ B cells, as both MZ and FO B cell populations express an identical Ag receptor.

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CD4 T cell priming in dendritic cell-deficient mice

Cited by 18 publications

References 40 publications

CD8 T cell priming by B lymphocytes is CD4 help dependent

CD8 T cell priming by B lymphocytes is CD4 help dependent

Role of T cell help and endoplasmic reticulum targeting in protective CTL response against influenza virus

Marginal Zone, but Not Follicular B Cells, Are Potent Activators of Naive CD4 T Cells

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