ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Expression of the leptin receptor outside of bone marrow-derived cells regulates tuberculosis control and lung macrophage MHC expression.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 27 citations in OpenAlex.
- Chemerin Exacerbates Pulmonary Inflammation in Type 2 Diabetes and Mycobacterium Tuberculosis Infection Comorbidity.Inflammation · 2025Article
- Insufficient CXCL13 secretion in leprosy foamy macrophages attenuates lymphocyte recruitment and antimicrobial protein production.Frontiers in immunology · 2025Article
- Article
- Interplay Between the Immune and Endocrine Systems in the Lung: Implications for TB Susceptibility.Frontiers in immunology · 2022Review
- Leptin signaling impairs macrophage defenses againstProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Exploring immunomodulation by endocrine changes in Lady Windermere syndrome.Clinical and experimental immunology · 2019Review
- Ablation of the leptin receptor in myeloid cells impairs pulmonary clearance of Streptococcus pneumoniae and alveolar macrophage bactericidal function.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Immunological roulette: Luck or something more? Considering the connections between host and environment in TB.Cellular & molecular immunology · 2018Review
- Soluble mediators regulating immunity in early life.Frontiers in immunology · 2014Review
- Leptin as regulator of pulmonary immune responses: involvement in respiratory diseases.Pulmonary pharmacology & therapeutics · 2013Review
- Leptin and mucosal immunity.Mucosal immunology · 2012Review
- Protection versus pathology in tuberculosis: recent insights.Current opinion in immunology · 2012Review
- The immunological life cycle of tuberculosis.Nature reviews. Immunology · 2012Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Leptin is a pleiotropic hormone proposed to link nutritional status to the development of strong Th1 immunity. Because Mycobacterium tuberculosis control is affected by starvation and diabetes, we studied the role of the leptin receptor in regulating distinct immune cells during chronic infection. Infected db/db mice, bearing a natural mutation in the leptin receptor, have a markedly increased bacterial load in their lungs when compared with that of their wild-type counterparts. In response to M. tuberculosis infection, db/db mice exhibited disorganized granulomas, neutrophilia, and reduced B cell migration to the lungs, correlating with dysfunctional lung chemokine responses that include XCL1, CCL2, CXCL1, CXCL2, and CXCL13. In a db/db lung, myeloid cells were delayed in their production of inducible NO synthase and had reduced expression of MHC I and II. Although the Th1 cell response developed normally in the absence of leptin signaling, production of pulmonary IFN-γ was delayed and ineffective. Surprisingly, a proper immune response took place in bone marrow (BM) chimeras lacking leptin receptor exclusively in BM-derived cells, indicating that leptin acts indirectly on immune cells to modulate the antituberculosis response and bacterial control. Together, these findings suggest that the pulmonary response to M. tuberculosis is affected by the host's nutritional status via the regulation of non-BM-derived cells, not through direct action of leptin on Th1 immunity.
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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.