scholarly journals Skin as a Peripheral Lymphoid Organ: Revisiting the Concept of Skin-Associated Lymphoid Tissues

2011 ◽  
Vol 131 (11) ◽  
pp. 2178-2185 ◽  
Author(s):  
Gyohei Egawa ◽  
Kenji Kabashima
Keyword(s):  
Lymphoid Organ ◽  
Lymphoid Tissues ◽  
Peripheral Lymphoid Organ

scholarly journals Peripheral CD103+ dendritic cells form a unified subset developmentally related to CD8α+ conventional dendritic cells

2010 ◽  
Vol 207 (4) ◽  
pp. 823-836 ◽  
Author(s):  
Brian T. Edelson ◽  
Wumesh KC ◽  
Richard Juang ◽  
Masako Kohyama ◽  
Loralyn A. Benoit ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Transcription Factor ◽  
Lymph Nodes ◽  
Sendai Virus ◽  
Pulmonary Inflammation ◽  
Lymphoid Organ ◽  
Contact Hypersensitivity ◽  
Lymphoid Tissues ◽  
Mesenteric Lymph Nodes ◽  
Normal Contact

Although CD103-expressing dendritic cells (DCs) are widely present in nonlymphoid tissues, the transcription factors controlling their development and their relationship to other DC subsets remain unclear. Mice lacking the transcription factor Batf3 have a defect in the development of CD8α+ conventional DCs (cDCs) within lymphoid tissues. We demonstrate that Batf3−/− mice also lack CD103+CD11b− DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draining lymph nodes. Notably, Batf3−/− mice displayed reduced priming of CD8 T cells after pulmonary Sendai virus infection, with increased pulmonary inflammation. In the MLNs and intestine, Batf3 deficiency resulted in the specific lack of CD103+CD11b− DCs, with the population of CD103+CD11b+ DCs remaining intact. Batf3−/− mice showed no evidence of spontaneous gastrointestinal inflammation and had a normal contact hypersensitivity (CHS) response, despite previous suggestions that CD103+ DCs were required for immune homeostasis in the gut and CHS. The relationship between CD8α+ cDCs and nonlymphoid CD103+ DCs implied by their shared dependence on Batf3 was further supported by similar patterns of gene expression and their shared developmental dependence on the transcription factor Irf8. These data provide evidence for a developmental relationship between lymphoid organ–resident CD8α+ cDCs and nonlymphoid CD103+ DCs.

Peripheral Lymphoid Organ

2016 ◽  
Author(s):  
Douglas M. Templeton ◽  
Michael Schwenk ◽  
Reinhild Klein ◽  
John H. Duffus
Keyword(s):  
Lymphoid Organ ◽  
Peripheral Lymphoid Organ

Expression of relB transcripts during lymphoid organ development: specific expression in dendritic antigen-presenting cells

Development ◽  
1993 ◽  
Vol 118 (4) ◽  
pp. 1221-1231 ◽  
Author(s):  
D. Carrasco ◽  
R.P. Ryseck ◽  
R. Bravo
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Signal Transduction Pathway ◽  
Antigen Presenting Cells ◽  
Lymphoid Organ ◽  
Lymphoid Tissues ◽  
Mouse Development ◽  
Specific Expression ◽  
Dendritic Cell Differentiation ◽  
Antigen Presenting

We have studied the expression of the relB gene during mouse development using in situ hybridization and immunocytochemical analysis. The results show that the expression of the relB gene is highly restricted to a subpopulation of cells that colonize the lymphoid tissues and that appear very late during the process of hematopoietic diversification. RNA transcripts of relB are very low or undetectable in early and late embryos. Low relB expression is observed in the thymus at late stages of embryogenesis but rapidly increases after birth. In adult lymphoid tissues, relB is detected in the medullary region of the thymus, the periarterial lymphatic sheaths of the spleen, and the deep cortex of the lymph nodes, which correspond to the regions where T cells of mature phenotype and interdigitating dendritic cells are present. Using double immunofluorescent labeling of thymic cell suspensions, we have identified the interdigitating dendritic cells as the target of RelB expression. These cells are part of a system of antigen-presenting cells that function in the induction of several immune responses, such as, tolerance, sensitization of MHC-restricted T cells, rejection of organ transplants and formation of T-dependent antibodies. Our observations indicate that RelB may play a particular role in the signal transduction pathway that regulate dendritic cell differentiation and its cellular responses.

Fine Structural Alterations in Thyroid Follicular Cells (FC) and Changes in Serum Thyroxine Produced by Feeding Polychlorinated Biphenyl (PCB) to Rats

1977 ◽  
Vol 35 ◽  
pp. 498-499
Author(s):  
W.T. Collins ◽  
Charles C. Capen ◽  
Louis Kasza
Keyword(s):  
Feed Efficiency ◽  
Polychlorinated Biphenyl ◽  
Serum Proteins ◽  
Skin Lesions ◽  
Hepatic Necrosis ◽  
Ultrastructural Changes ◽  
Lymphoid Tissues ◽  
Heat Transfer Fluids ◽  
Thyroid Follicular Cells ◽  
Peripheral Metabolism

The widespread contamination of the environment with PCB, a compound used extensively by industry in hydraulic and heat transfer fluids as well as plasticizers and solvents in adhesives and sealants, has resulted in detectable tissue levels in a large portion of the human population, domestic animals, and wildlife. Intoxication with PCB produces severe hepatic necrosis, degeneration of lymphoid tissues and kidney, skin lesions, decreased reproductive performance, reduced feed efficiency, and decreased weight gain. PCB also has been reported to reduce the binding of thyroid hormone to serum proteins and enhance the peripheral metabolism of thyroxine with increased excretion of thyroxine-glucuronide in the bile (Bastomsky, Endocrinology 95: 1150-1155, 1974).The objectives of this investigation were (1) to investigate the histopathologic, histochemical, and ultrastructural changes in thyroid FC produced by the acute (4 week) and chronic (12 week) administration of low (50 ppm) and high (500 ppm) doses of PCB to rats, (2) to correlate these alterations to changes in serum immunoreactive thyroxine concentration, and (3) to investigate the persistence of the effects of PCB on the thyroid gland.

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