ArticleThe Journal of experimental medicine1999
Mice lacking expression of secondary lymphoid organ chemokine have defects in lymphocyte homing and dendritic cell localization.
Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 324 papers, 1 of them a synthesis that pooled it.
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Who cites it
324 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,013 citations in OpenAlex.
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- Maturation of Tertiary Lymphoid Structures.Methods in molecular biology (Clifton, N.J.) · 2025Review
- [Assessment of baseline CCL19Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
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- Chemokine CCL19 promotes type 2 T-cell differentiation and allergic airway inflammation.The Journal of allergy and clinical immunology · 2024Article
- A phase 1 trial of human telomerase reverse transcriptase (hTERT) vaccination combined with therapeutic strategies to control immune-suppressor mechanisms.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Advances in understanding of dendritic cell in the pathogenesis of acute kidney injury.Frontiers in immunology · 2024Review
264 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary lymphoid organ chemokine (SLC) is expressed in high endothelial venules and in T cell zones of spleen and lymph nodes (LNs) and strongly attracts naive T cells. In mice homozygous for the paucity of lymph node T cell (plt) mutation, naive T cells fail to home to LNs or the lymphoid regions of spleen. Here we demonstrate that expression of SLC is undetectable in plt mice. In addition to the defect in T cell homing, we demonstrate that dendritic cells (DCs) fail to accumulate in spleen and LN T cell zones of plt mice. DC migration to LNs after contact sensitization is also substantially reduced. The physiologic significance of these abnormalities in plt mice is indicated by a markedly increased sensitivity to infection with murine hepatitis virus. The plt mutation maps to the SLC locus; however, the sequence of SLC introns and exons in plt mice is normal. These findings suggest that the abnormalities in plt mice are due to a genetic defect in the expression of SLC and that SLC mediates the entry of naive T cells and antigen-stimulated DCs into the T cell zones of secondary lymphoid organs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.