Thymic nurse cells—Ia-bearing epithelium involved in T-lymphocyte differentiation?

Wekerle, Hartmut; Ketelsen, Uwe‐Peter

doi:10.1038/283402a0

Cited by 250 publications

(123 citation statements)

References 12 publications

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“…Interestingly, increased galectin-3 expression was also observed on B cells from T. cruzi-infected mice, and this expression correlated with the ability of this protein to favor a memory B-cell phenotype. 33 Two models of thymic epithelial cells, the IT-76M1 TEC line 34 -36 and primary cultures of the TNCs, 25 were used in this study to examine galectin accumulation on infection with T. cruzi. In both cases, galectin-3 (but not galectin-1) accumulated after exposure to the parasite.…”

Section: Discussionmentioning

confidence: 99%

“…Cultures were then fixed in 4% buffered paraformaldehyde for 5 minutes and processed for immunocytochemistry. TNCs, isolated from thymuses of control or infected mice as previously described, 25,26 were plated onto sterile glass slides and cultured for 35 to 60 hours. Adhered TNCs were then washed with phosphate-buffered saline (PBS), fixed as mentioned above and processed for immunocytochemistry.…”

Section: Tissues and Cell Culturesmentioning

confidence: 99%

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Altered Expression of Galectin-3 Induces Cortical Thymocyte Depletion and Premature Exit of Immature Thymocytes during Trypanosoma cruzi Infection

Silva

Lorenzato

Nihei

et al. 2007

The American Journal of Pathology

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During acute infection with Trypanosoma cruzi, the causative agent of Chagas' disease, the thymus undergoes intense atrophy followed by a premature escape of CD4 ؉ CD8 ؉ immature cortical thymocytes. Here we report a pivotal role for the endogenous lectin galectin-3 in accelerating death of thymocytes and migration of these cells away from the thymus after T. cruzi infection. We observed a pronounced increase in galectin-3 expression that paralleled the extensive depletion of CD4 ؉ CD8 ؉ immature thymocytes after infection. In vitro, recombinant galectin-3 induced increased levels of death in cortical immature thymocytes. Consistent with the role of galectin-3 in promoting cell death, thymuses from gal-3 ؊/؊ mice did not show cortical thymocyte depletion after parasite infection in vivo. In addition, galectin-3 accelerated laminin-driven CD4 ؉ CD8 ؉ thymocyte migration in vitro and in vivo induced exportation of CD4 ؉ CD8 ؉ cells from the thymus to the peripheral compartment. Our findings provide evidence of a novel role for galectin-3 in the regulation of thymus physiology and identify a potential mechanism based on proteinglycan interactions in thymic atrophy associated with acute T. cruzi infection.

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Section: Discussionmentioning

confidence: 99%

Section: Tissues and Cell Culturesmentioning

confidence: 99%

Altered Expression of Galectin-3 Induces Cortical Thymocyte Depletion and Premature Exit of Immature Thymocytes during Trypanosoma cruzi Infection

Silva

Lorenzato

Nihei

et al. 2007

The American Journal of Pathology

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“…TNCs and cultures of nonepithelial phagocytic cells of the thymic reticulum (PTR) were obtained as described before. [48][49][50] …”

Section: Methodsmentioning

confidence: 99%

Identification, structural characterization, and tissue distribution of Tsg-5: a new TNF-stimulated gene

Abrantes

Pires²,

Carvalho

et al. 2003

Genes Immun

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Using DDRT-PCR, we compared the mRNA content of untreated and TNF-treated mouse embryonic fibroblasts (MEFs). Among differentially represented fragments, we identified and cloned a novel TNF-stimulated gene named Tsg-5. This gene, mapped to mouse chromosome 14, has three exons that can be alternatively spliced giving rise to two mRNA species, one spanning three exons and another that skips the second exon. Analysis of full-length Tsg-5 cDNA revealed a potential start codon within exon 2 encoding an ORF of 40 amino-acids. No homology with known mouse or human sequences, neither at the nucleotide nor at the amino-acid level could be found in public databases. In MEFs, Tsg-5 is induced by tumor necrossis factora (TNF) and IL-1b, albeit with distinct kinetics. TNF-induced Tsg-5 expression is NF-kB-dependent as it was inhibited by MG132, lactacystin, Bay 11-7083, and Bay 11-7085. Analysis of Tsg-5 expression in vivo revealed that the gene and its encoded polypeptide are constitutively expressed in the thymus and ovary, whereas, in LPS-treated mice, Tsg-5 mRNA can be detected in the spleen, lung, and brain. Our data suggest that Tsg-5 encodes a new, rare transcript, with a very tight regulation of expression and differential splicing.

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“…Interaction of precursor T cells with H-2 Iabearing cells appears to be necessary for appropriate maturation of T helper cells. This, especially, suggests that thymic selection concerns class II MHC specifically (46,47). Indeed, the presence of class II (but not class I) MHC antigens on the cortical epithelium (48, 49) might suggest selection for class IIreactive cells.…”

Section: Discussionmentioning

confidence: 99%

Thymus dictates major histocompatibility complex (MHC) specificity and immune response gene phenotype of class II MHC-restricted T cells but not of class I MHC-restricted T cells.

Kast¹,

Waal²,

Melief³

1984

The Journal of Experimental Medicine

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Athymic H-2b nude mice received grafts from C57BL/6 (Sendai virus and H-Y antigen cytotoxic T lymphocyte [CTL] responder type), bm1 (H-2Kb mutant, Sendai CTL nonresponder type), or bm12 (H-21-A mutant, H-Y CTL nonresponder type) neonates. In observations of the CTL response to H-Y, both recipients and thymus donors were female. All types of thymus engraftment resulted in mature H-2b splenic T lymphocyte surface phenotype in nude hosts. T cell immunocompetence (as measured by major histocompatibility complex [MHC] CTL responses to allogeneic cells) was restored, and induced nonresponsiveness to the MHC determinants of the engrafted thymus in the nude host. The CTL reaction to Sendai virus in both responder type C57BL/6 and nonresponder type bm1 neonatal thymuses allowed maturation of Sendai-specific, H-2Kb-restricted CTL. For the CTL reaction to H-Y, only responder type C57BL/6 thymuses restored the CTL response, whereas this was not achieved with thymuses from nonresponder type bm12 neonatal females. Results of double thymus (B6 and bm12) engraftment excluded the possibility that this latter effect was caused by suppression. In addition, athymic bm1 mice were engrafted with thymuses from either B6 (Sendai CTL responder type) or syngeneic bm1 neonates (Sendai CTL nonresponder type). Again, both types of neonate thymuses restored T cell competence as measured by MHC/CTL responses to allogeneic cells. However, neither responder B6 nor nonresponder bm1 neonate thymus grafts allowed maturation of Sendai-specific CTL. In conclusion, the thymus dictates MHC specificity and immune response gene phenotype of T cells restricted to class II MHC molecules but not of T cells restricted to class I MHC molecules.

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Thymic nurse cells—Ia-bearing epithelium involved in T-lymphocyte differentiation?

Cited by 250 publications

References 12 publications

Altered Expression of Galectin-3 Induces Cortical Thymocyte Depletion and Premature Exit of Immature Thymocytes during Trypanosoma cruzi Infection

Altered Expression of Galectin-3 Induces Cortical Thymocyte Depletion and Premature Exit of Immature Thymocytes during Trypanosoma cruzi Infection

Identification, structural characterization, and tissue distribution of Tsg-5: a new TNF-stimulated gene

Thymus dictates major histocompatibility complex (MHC) specificity and immune response gene phenotype of class II MHC-restricted T cells but not of class I MHC-restricted T cells.

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