ReviewLung1994
Adhesion molecules in lung diseases.
Review in Lung, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 49 citations in OpenAlex.
- Immune mechanisms and novel therapies for idiopathic pulmonary fibrosis.Pharmaceutical science advances · 2024Review
- Adhesion Molecules in Lung Inflammation from Repeated Glyphosate Exposures.International journal of environmental research and public health · 2023Article
- The relationship between the serum intercellular adhesion molecule-1 level and the prognosis of the disease in lung cancer.The Korean journal of internal medicine · 2004Article
- Possible role of L-selectin in T lymphocyte alveolitis in patients with active pulmonary sarcoidosis.Clinical and experimental immunology · 2000Article
- Selective inflammatory response induced by intratracheal and intravenous administration of poly-L-arginine in guinea pig lungs.Inflammation · 1999Article
- High frequency oscillatory ventilation attenuates the activation of alveolar macrophages and neutrophils in lung injury.Critical care (London, England) · 1998Article
- Adhesion molecules in vernal keratoconjunctivitis.The British journal of ophthalmology · 1997Article
- Article
- Endothelial modification of pulmonary vascular tone.Intensive care medicine · 1996Review
- Imbalance of pro- and anti-inflammatory cytokines in pulmonary sarcoidosis.Mediators of inflammation · 1996Article
- Lymphocytes in the lung: an often neglected cell. Numbers, characterization and compartmentalization.Anatomy and embryology · 1995Review
- Increased expression of intercellular adhesion molecule-1 (ICAM-1) in a murine model of pulmonary eosinophilia and high IgE level.Clinical and experimental immunology · 1995Article
- Article
- Pulmonary immune responses induced in BALB/c mice by Paracoccidioides brasiliensis conidia.MycopathologiaReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human body possesses highly specialized cellular defense mechanisms that, when activated pathologically, can induce a number of immunologic disorders. For a normal cellular immune response, the following conditions must be fulfilled: (1) accumulation of white blood cells, (2) their diapedesis through the vessel walls of the inflammatory area affected by an injurious agent, and (3) normal cellular effector functions in the tissue. This cascade of inflammatory processes has recently been shown to be regulated by a group of molecules that are termed adhesion molecules and consist of three subfamilies: selectins, the immunoglobulin supergene family, and integrins. The cellular functions influenced by adhesion molecules include, among others, cytotoxic T-cell responses, CD4-dependent activation of B lymphocytes by T lymphocytes, activation of granulocytes and macrophages, phagocytosis of opsonized particles by monocytes, macrophages, and granulocytes, antigen-presenting function of macrophages, their antibody-dependent cytotoxicity, initiation of a respiratory burst by white blood cells, and activation of fibroblasts. Studies performed in recent years have shown that pathogenetically relevant changes in the expression and function of adhesion molecules are involved in a variety of pulmonary diseases. These changes include the accumulation and activation of alveolar macrophages in smokers, experimentally induced bronchial hyperreactivity in bronchial asthma, accumulation of eosinophils in allergic rhinitis, bleomycin-induced pulmonary fibrosis, binding of viruses and bacteria to respiratory mucosa, and various mechanisms of acute damage to pulmonary parenchyma. Though their role in tumor development is still unclear, adhesion molecules are obviously involved in determining the route and organotropism of metastases. Further studies of the function of adhesion molecules in pulmonary diseases will contribute to our understanding of the pathomechanisms of these diseases and, through the development of specific antibodies, may provide attractive new therapeutic approaches to problems for which treatment is not yet available.
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.