TNF Receptor-1 Is Required for the Formation of Splenic Compartments during Adult, but Not Embryonic Life
Autor: | Karola Klaperski, Kathrin Kalies, Babett Baraniec, Maike Blessenohl, Živana Milićević, Novica M. Milićević, Jürgen Westermann, Katja Bieber, Klaus Nohroudi, Carl F. Ware |
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Rok vydání: | 2011 |
Předmět: |
Male
Aging Pathology medicine.medical_specialty T cell Immunology B-Lymphocyte Subsets Spleen Biology Mice Fetus Lymphotoxin beta Receptor T-Lymphocyte Subsets medicine Animals Immunology and Allergy B cell Laser capture microdissection Mice Knockout respiratory system Marginal zone Cell Compartmentation Cell biology Mice Inbred C57BL medicine.anatomical_structure Lymphotoxin Lymphatic system Receptors Tumor Necrosis Factor Type I Splenic Tissue Female Signal Transduction |
Zdroj: | The Journal of Immunology. 186:1486-1494 |
ISSN: | 1550-6606 0022-1767 |
Popis: | Lymphotoxin β-receptor (LTβR) and TNF receptor-1 (TNFR1) are important for the development of secondary lymphoid organs during embryonic life. The significance of LTβR and TNFR1 for the formation of lymphoid tissue during adult life is not well understood. Immunohistochemistry, morphometry, flow cytometry, and laser microdissection were used to compare wild-type, LTβR−/−, TNFR1−/− spleens with splenic tissue that has been newly formed 8 wk after avascular implantation into adult mice. During ontogeny, LTβR is sufficient to induce formation of the marginal zone, similar-sized T and B cell zones, and a mixed T/B cell zone that completely surrounded the T cell zone. Strikingly, in adult mice, the formation of splenic compartments required both LTβR and TNFR1 expression, demonstrating that the molecular requirements for lymphoid tissue formation are different during embryonic and adult life. Thus, interfering with the TNFR1 pathway offers the possibility to selectively block the formation of ectopic lymphoid tissue and at the same time to spare secondary lymphoid organs such as spleen and lymph nodes. This opens a new perspective for the treatment of autoimmune and inflammatory diseases. |
Databáze: | OpenAIRE |
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