Identification and clinical association of anti-cytokeratin 18 autoantibody in COPD

Kuo, Yung-Bin; Chang, C. Allen; Wu, Yao‐Kuang; Hsieh, Meng‐Jer; Tsai, Chung-Hsien; Chen, Kuei-Tien; Chen, Chun-Yu; Chan, Err–Cheng

doi:10.1016/j.imlet.2009.12.017

Cited by 29 publications

(24 citation statements)

References 47 publications

(60 reference statements)

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“…These antigens are vomeromodulin in mice, or a related protein, LPLUNC1 in humans [24], and KCNRG [23, 45], both of which are absent from the autoantigen array employed in this study. Additionally, cytokeratin 18 antibodies have been shown to be present and correlate with disease progression in COPD and were not included in this array [13]. Finally, post-translational modifications have been proposed as an origin of neo-self antigens, and a recent study has demonstrated the presence of antibodies reactive to modified self-proteins in COPD [12].…”

Section: Discussionmentioning

confidence: 99%

COPD is associated with production of autoantibodies to a broad spectrum of self-antigens, correlative with disease phenotype

Packard

Cosgrove

et al. 2012

Immunol Res

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The role of autoimmune pathology in development and progression of chronic obstructive pulmonary disease (COPD) is becoming increasingly appreciated. In this study, we identified serum autoantibody reactivities associated with chronic bronchitis or emphysema, as well as systemic autoimmunity and associated lung disease. Using autoantigen array analysis, we demonstrated that COPD patients produce autoantibodies reactive to a broad spectrum of self-antigens. Further, the level and reactivities of these antibodies, or autoantibody profile, correlated with disease phenotype. Patients with emphysema produced autoantibodies of higher titer and reactive to an increased number of array antigens. Strikingly, the autoantibody reactivities observed in emphysema were increased over those detected in rheumatoid arthritis patients, and included similar reactivities to those associated with lupus. These findings raise the possibility that autoantibody profiles may be used to determine COPD risk, as well as provide a diagnostic and prognostic tool. They shed light on the heterogeneity of autoantibody reactivities associated with COPD phenotype and could be of use in the personalization of medical treatment, including determining and monitoring therapeutic interventions.

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Section: Discussionmentioning

confidence: 99%

COPD is associated with production of autoantibodies to a broad spectrum of self-antigens, correlative with disease phenotype

Packard

Cosgrove

et al. 2012

Immunol Res

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“…A high prevalence of anti-Hep-2 epithelial cell autoantibodies has been shown in patients with COPD [1,2], as well as autoantibodies against airway epithelial cells [1], endothelial cells [3], lung elastin [4], several immunogenic peptides [5] and cytokeratin 18 [6]. The most convincing evidence for an autoimmune response in COPD was provided by LEE et al [4].…”

Section: To the Editorsmentioning

confidence: 99%

The search for autoantibodies against elastin, collagen and decorin in COPD

Brandsma

Kerstjens

Geerlings³

et al. 2011

European Respiratory Journal

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“…Supporting evidence comes from the presence of antinuclear antibodies11 and circulating IgG antibodies against pulmonary epithelial cells,12 endothelial cells13 and extracellular matrix proteins14 in patients with COPD. However, it remains unclear whether these antibodies should be regarded as bystander, protective or pathogenic antibodies as they may be equally found in healthy smokers.…”

Section: Introductionmentioning

confidence: 99%

Antielastin B-cell and T-cell immunity in patients with chronic obstructive pulmonary disease

Rinaldi

Lehouck

Heulens

et al. 2012

Thorax

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Rationale Antielastin autoimmunity has been hypothesised to drive disease progression in chronic obstructive pulmonary disease (COPD). The proposed mechanism is currently disputed by conflicting data. The authors aimed to explore antibody responses against elastin in a large and extensively characterised COPD population and to assess elastin-specific peripheral T-cell reactivity in a representative subgroup. Methods Antielastin antibodies were analysed with indirect ELISA on the plasma of 320 patients with COPD (Global Initiative for Chronic Obstructive Lung Disease 1e4) and 143 smoking controls. In a second group of 40 patients with COPD and smoking controls, T-cell responses against extracellular matrix (elastin, collagen I and collagen V) were determined with enzyme-linked immunosorbent spot (EliSpot) (interferon g (IFNg) and interleukin-2) on peripheral blood mononuclear cells and compared with the responses of 11 never-smoking controls. Results Antielastin antibody titres were not elevated in patients with COPD compared with smoking controls and even decreased significantly with increasing severity of COPD (p<0.001). Lower antielastin antibody titres were also found in a subgroup of patients with CT-proven emphysema. Elastin-specific INFg-mediated T helper 1 responses could not be revealed in smoking subjects with and without COPD. Collagen I-mediated T-cell responses were also absent, which contrasted with a significant increased anticollagen V response in the smoking controls and patients with COPD compared with the never smokers (p¼0.008). Collagen V-mediated T-cell responses could not discriminate between patients with COPD and smoking controls. Conclusion A systemic immune response against elastin could not be identified in patients with COPD. By contrast, collagen V-mediated autoimmunity was increased in the subgroup of smokers and may potentially contribute to the pathogenesis of COPD.

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Identification and clinical association of anti-cytokeratin 18 autoantibody in COPD

Cited by 29 publications

References 47 publications

COPD is associated with production of autoantibodies to a broad spectrum of self-antigens, correlative with disease phenotype

COPD is associated with production of autoantibodies to a broad spectrum of self-antigens, correlative with disease phenotype

The search for autoantibodies against elastin, collagen and decorin in COPD

Antielastin B-cell and T-cell immunity in patients with chronic obstructive pulmonary disease

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