The Possibility of B‐Cell‐Dependent T‐Cell Development

Keshavarzi, Sassan; Rietz, Cecilia; Simões, Sérgio; Shih, S.E.; Platt, Jeffrey L.; Wong, Jamie; Wabl, Matthias; Cascalho, Marília

doi:10.1046/j.1365-3083.2003.01257.x

Cited by 14 publications

(17 citation statements)

References 43 publications

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“…QM mice have 80% of B cells that are 4-hydroxy-3-nitrophenylacetate specific (16). Monoclonal B cell-T cell mice have monoclonal B and T cell compartments; the T cells express an ␣␤ DO 11.10 transgenic cell receptor restricted to MHC class II b (11). JH Ϫ/Ϫ and QM mice were bred and all mice were housed in a specific pathogen-free facility at the Mayo Clinic.…”

Section: Strains Of Micementioning

confidence: 99%

“…Defective responses to intracellular pathogens suggest the possibility that, in addition to hypogammaglobulinemia, individuals and mice with B cell deficiency may suffer intrinsic abnormalities in the T cell compartment. We recently found that B cell-deficient mice have a remarkable decrease in the number and diversity of thymocytes (11,12) and hypothesized that defects in cell-mediated immunity could result from contraction of the TCR repertoire. Because each TCR recognizes a limited number of different peptides associated with MHC, the recognition of diverse Ags, even allowing for crossreactivity, is thought to reflect the diversity of the TCR repertoire.…”

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confidence: 99%

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Fitness of Cell-Mediated Immunity Independent of Repertoire Diversity

AbuAttieh¹,

Rebrovich²,

Wettstein³

et al. 2007

The Journal of Immunology

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Fitness of cell-mediated immunity is thought to depend on TCR diversity; however, this concept has not been tested formally. We tested the concept using JH−/− mice that lack B cells and have TCR Vβ diversity <1% that of wild-type mice and quasimonoclonal (QM) mice with oligoclonal B cells and TCR Vβ diversity 7% that of wild-type mice. Despite having a TCR repertoire contracted >99% and defective lymphoid organogenesis, JH−/− mice rejected H-Y-incompatible skin grafts as rapidly as wild-type mice. JH−/− mice exhibited T cell priming by peptide and delayed-type hypersensitivity, although these responses were less than normal owing either to TCR repertoire contraction or defective lymphoid organogenesis. QM mice with TCR diversity contracted >90%, and normal lymphoid organs rejected H-Y incompatible skin grafts as rapidly as wild type mice and exhibited normal T cell priming and normal delayed-type hypersensitivity reactions. QM mice also resisted Pneumocystis murina like wild-type mice. Thus, cell-mediated immunity can function normally despite contractions of TCR diversity >90% and possibly >99%.

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Section: Strains Of Micementioning

confidence: 99%

mentioning

confidence: 99%

Fitness of Cell-Mediated Immunity Independent of Repertoire Diversity

AbuAttieh¹,

Rebrovich²,

Wettstein³

et al. 2007

The Journal of Immunology

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“…Low levels of transgenic B29-k5D transcripts but no protein (data not shown) was detectable in the thymus (Fig. 6A), which could be explained by crosslineage expression of the B29 gene in developing thymoctyes [24] and the presence of a minor fraction of thymus-resident B lineage cells [25]. Unexpectedly, in several independent lines, we also detected transgene expression by RT-PCR at low levels, similar to those in bone marrow and spleen, in non-lymphoid organs, such as testis, kidney and brain (Fig.…”

Section: Discussionmentioning

confidence: 95%

“…6A, B, upper panels). While transgenic transcripts in the thymus can be explained by crosslineage expression of the B29 gene in developing thymoctyes [24] and the presence of a minor fraction of thymus-resident B cells [25], the other organs were devoid of endogenous Ig-b transcripts and, hence, of contaminating B or T lymphoid cells (Fig. 6A, middle panel).…”

Section: Altered Tissue Restriction Of B29-k5d Transgenesmentioning

confidence: 99%

Genomic suppression of murine B29/Ig‐β promoter‐driven transgenes

et al. 2006

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Immunoglobulin b (Ig-b) is a critical signal transducer of precursor B cell and B cell receptors. B29, the gene coding for Ig-b, is switched on in progenitor B cells and expressed until the terminal stage of antibody-producing plasma cells. Although several cis-acting elements and transcription factors required for B29 expression have been characterized in cell lines, the in vivo significance of individual motifs located in the 1.2-kb promoter region remained unclear. To address whether this region drives B lineage-specific expression in mice as efficiently as in transfected cell lines, we established transgenic animals carrying the B29 promoter fused to either enhanced green fluorescent protein (EGFP) or the precursor B cell receptor component k5. Surprisingly, only minimal levels of B29-derived transcripts were produced in B lymphoid tissues of several independent transgenic lines, and the respective proteins were below the detection limit. In addition, transgenic transcripts were found in testis, kidney and brain. Hence, the 1.2-kb-sized B29 promoter does not define a strong, B lineage-restricted expression unit when randomly integrated into the genome and passed through the murine germ line. Therefore, yet unidentified genomic locus control elements are required to efficiently drive B29 expression in B lymphocytes.

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“…Mice with monoclonal T cells expressing the DO 11.10 (DO) TCR (DO-T) which recognize a peptide of ovalbumin in the context of MHC class II d were interbred with monoclonal B cell mice [27,28]. We studied the development of DO-T cells in mice with and without monoclonal B cells, the monoclonal B-T and the monoclonal T mice, respectively [29]. In the monoclonal T mice, the DO-T cells are deleted in the thymus by binding to MHC class II b presenting nominal endogenous peptides, and these have only rare conventional CD4+ T cells in the periphery.…”

Section: Monoclonal B Cells Counteract Negative Selection Of Transgenmentioning

confidence: 99%

B Cells and B Cell Products – Helping to Restore Cellular Immunity?

Cascalho¹,

Platt²

2006

Transfus Med Hemother

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T cells that provide vital protection against tumors, viruses, and intracellular bacteria are thought to develop independently of B cells. However, recent discoveries suggest that development of T cells depends on B cells. One way B cells promote T cell development is by providing diverse peptides that may promote positive selection of thymocytes. Diverse peptides and B cells help in diversification of the T cell receptor repertoire and may decrease cross-reactivity in the mature T cell compartment. These new insights may provide the basis for the design of novel therapeutics.

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The Possibility of B‐Cell‐Dependent T‐Cell Development

Cited by 14 publications

References 43 publications

Fitness of Cell-Mediated Immunity Independent of Repertoire Diversity

Fitness of Cell-Mediated Immunity Independent of Repertoire Diversity

Genomic suppression of murine B29/Ig‐β promoter‐driven transgenes

B Cells and B Cell Products – Helping to Restore Cellular Immunity?

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