CD8+ T lymphocytes in lung tissue from patients with idiopathic pulmonary fibrosis

Daniil, Zoe; Kitsanta, Panagiota; Kapotsis, G.E.; Mathioudaki, Maria; Kollintza, Androniki; Karatza, Marilena; Milic–Emili, J.; Roussos, Charis; Papiris, Spyros

doi:10.1186/1465-9921-6-81

Cited by 59 publications

(62 citation statements)

References 51 publications

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“…Nonetheless, the lungs of IPF patients display an interstitial infiltrate consisting primarily of mononuclear cells, with a recent investigation indicating that CD3 T cells and plasma cells constituted the most frequent cell types [129,130]. In one study, CD4 T cells were found primarily in aggregates in or near lymphoid follicles, whereas CD8 T cells were diffusely scattered throughout the parenchyma [130]. This is consistent with earlier results in patients with CFA or UIP, though they were not classified according to ATS criteria [131,132].…”

Section: Mediators Of Fibrosismentioning

confidence: 98%

Idiopathic Pulmonary Fibrosis—an Epidemiological and Pathological Review

Borchers

Chang²,

Keen

et al. 2010

Clinic Rev Allerg Immunol

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Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease (ILD) affecting the pulmonary interstitium. Other forms of interstitial lung disease exist, and in some cases, an environmental etiology can be delineated. The diagnosis of IPF is typically established by high-resolution CT scan. IPF tends to have a worse prognosis than other forms of ILD. Familial cases of IPF also exist, suggesting a genetic predisposition; telomerase mutations have been observed to occur in familial IPF, which may also explain the increase in IPF with advancing age. Alveolar epithelial cells are believed to be the primary target of environmental agents that have been putatively associated with IPF. These agents may include toxins, viruses, or the autoantibodies found in collagen vascular diseases. The mechanism of disease is still unclear in IPF, but aberrations in fibroblast differentiation, activation, and proliferation may play a role. Epithelial-mesenchymal transition may also be an important factor in the pathogenesis, as it may lead to accumulation of fibroblasts in the lung and a disruption of normal tissue structure. Abnormalities in other components of the immune system, including T cells, B cells, and dendritic cells, as well as the development of ectopic lymphoid tissue, have also been observed to occur in IPF and may play a role in the stimulation of fibrosis that is a hallmark of the disease. It is becoming increasingly clear that the pathogenesis of IPF is indeed a complex and convoluted process that involves numerous cell types and humoral factors.

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Section: Mediators Of Fibrosismentioning

confidence: 98%

Idiopathic Pulmonary Fibrosis—an Epidemiological and Pathological Review

Borchers

Chang²,

Keen

et al. 2010

Clinic Rev Allerg Immunol

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“…It is known that smoking cessation seems to rapidly restore the alveolar-capillary barrier integrity [57] and this is probably the reason why healthy ex-smokers presented with similar serum levels of SP-A and SP-D. However, this was not the case in patients with emphysema, fibrosis or CPFE in which circulating SP levels did not differ between current smokers and current non-smokers and it seems that the established lung inflammation in both pulmonary emphysema [58][59][60][61] and fibrosis [62][63][64][65] continues despite smoking cessation. Increased serum SP-A and SP-D levels in current smokers might be an early indicator of an ongoing parenchymal damage which might lead to the development of lung disease.…”

Section: Discussionmentioning

confidence: 65%

Serum levels of surfactant proteins in patients with combined pulmonary fibrosis and emphysema (CPFE)

Papaioannou

Κostikas

Papadaki

et al. 2015

1.5 Diffuse Parenchymal Lung Disease

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“…22 Furthermore, increased CD8 + T-cell density in the pulmonary interstitium and the downregulation of serum CD28 CD4 + cells both correlate with progressive disease. 52,132 These findings provide insight into the complex pathogenesis of IPF and the plethora of 'inflammatory' biomarkers that potentially have clinical relevance.…”

Section: Adaptive Immunity and Inflammation In Idiopathic Pulmonary Fmentioning

confidence: 99%

Molecular classification of idiopathic pulmonary fibrosis: Personalized medicine, genetics and biomarkers

2015

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Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive fibrotic lung disease associated with high morbidity and poor survival. Characterized by substantial disease heterogeneity, the diagnostic considerations, clinical course and treatment response in individual patients can be variable. In the past decade, with the advent of high-throughput proteomic and genomic technologies, our understanding of the pathogenesis of IPF has greatly improved and has led to the recognition of novel treatment targets and numerous putative biomarkers. Molecular biomarkers with mechanistic plausibility are highly desired in IPF, where they have the potential to accelerate drug development, facilitate early detection in susceptible individuals, improve prognostic accuracy and inform treatment recommendations. Although the search for candidate biomarkers remains in its infancy, attractive targets such as MUC5B and MPP7 have already been validated in large cohorts and have demonstrated their potential to improve clinical predictors beyond that of routine clinical practices. The discovery and implementation of future biomarkers will face many challenges, but with strong collaborative efforts among scientists, clinicians and the industry the ultimate goal of personalized medicine may be realized.

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CD8+ T lymphocytes in lung tissue from patients with idiopathic pulmonary fibrosis

Cited by 59 publications

References 51 publications

Idiopathic Pulmonary Fibrosis—an Epidemiological and Pathological Review

Idiopathic Pulmonary Fibrosis—an Epidemiological and Pathological Review

Serum levels of surfactant proteins in patients with combined pulmonary fibrosis and emphysema (CPFE)

Molecular classification of idiopathic pulmonary fibrosis: Personalized medicine, genetics and biomarkers

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