ArticleImmunology1997
Autocrine expression of interleukin-7 rescues lymphoid expansion in interleukin-7-deficient mice.
Article in Immunology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 17 citations in OpenAlex.
- Interleukin-7 induces recruitment of monocytes/macrophages to endothelium.European heart journal · 2012Article
- Progress in multiple sclerosis genetics.Current genomics · 2012Article
- Osteoblast-specific overexpression of human interleukin-7 rescues the bone mass phenotype of interleukin-7-deficient female mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2012Article
- Comparison of AAV/IL-7 autocrine (T cell) versus paracrine (DC) gene delivery for enhancing CTL stimulation and function.Cancer immunology, immunotherapy : CII · 2010Article
- Functional deficiency in IL-7 caused by an N-ethyl-N-nitrosourea-induced point mutation.Genetics · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The murine interleukin-7 (IL-7) gene was disrupted to examine the role of IL-7 in the lymphoid system. Expansion of lymphoid cells is sharply curtailed in IL-7-deficient mice. This is evident in a dramatic reduction but not elimination of lymphoid cells in the thymus, bone marrow and spleen. The few thymocytes present express CD4 and/or CD8 markers associated with T-cell maturation. Similarly, a limited number of B cells detected in the bone marrow rearrange and express immunoglobulin genes. Small but distinct populations of B and T cells are found in the spleens of IL-7-deficient mice. Thus the signal transmitted by IL-7 plays a central role in the expansion of lymphocytes while it is not absolutely required for their maturation. A transgene that directs expression of IL-7 to lymphoid cells was found to restore the numbers of thymocytes, bone marrow B-cell progenitors and splenic lymphocytes of IL-7-deficient mice to approximately normal levels. This genetic complementation confirms that the lymphoid defect is specifically due to the absence of IL-7 and demonstrates that the expansion of lymphoid cells in an organism is regulated by their exposure to IL-7.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.