The effect of CTLA-4Ig, a CD28/B7 antagonist, on the lung inflammation and T cell subset profile during murine hypersensitivity pneumonitis

Jiménez-Álvarez, Luis Armando; Arreola, José Luis; Ramírez-Martínez, Gustavo; Ortiz‐Quintero, Blanca; Gaxiola, Miguel; Reynoso-Robles, Rafael; Ávila‐Moreno, Federico; Urrea, Francisco; Pardo, Annie; Selman, Moisés; Zúñiga, Joaquı́n

doi:10.1016/j.yexmp.2011.09.010

Cited by 17 publications

(13 citation statements)

References 36 publications

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“…This is in line with data reported in the model of murine hypersensitivity pneumonitis, in which mice treated with abatacept exhibited a decreased number of T cells in the bronchoalveolar lavage 25. Decreased T-cell activation and infiltration may lead to decreased resident fibroblast activation in lesional skin, which is consistent with the reduction of TGF-β signalling and myofibroblast counts in abatacept-treated mice upon bleomycin challenge.…”

Section: Discussionsupporting

confidence: 90%

Treatment with abatacept prevents experimental dermal fibrosis and induces regression of established inflammation-driven fibrosis

et al. 2016

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Section: Discussionsupporting

confidence: 90%

Treatment with abatacept prevents experimental dermal fibrosis and induces regression of established inflammation-driven fibrosis

et al. 2016

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“…However, we see no increase in Tregs in WT or Cd103 -/- mice after SR exposure. Other studies have analyzed Tregs in response to SR and found an increase of this cell population in the lung [41, 42], but their model uses higher quantities of SR, which could explain the discrepancies between our studies. Our results therefore suggest that CD103 expression does not impact the Tregs response to SR antigen and that the exacerbation phenotype is not caused by a dysregulation of Tregs in Cd103 -/- mice.…”

Section: Discussioncontrasting

confidence: 76%

Hypersensitivity pneumonitis onset and severity is regulated by CD103 dendritic cell expression

et al. 2017

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BackgroundPulmonary dendritic cells drive lung responses to foreign antigens, including Saccharopolyspora rectivirgula, a causative agent of hypersensitivity pneumonitis. While the airway inflammatory mechanisms involved in hypersensitivity pneumonitis are well described, the mechanisms leading to the break in homeostasis and hypersensitivity pneumonitis onset are not well-described, and could involve CD103+ dendritic cells, which are found at baseline and during inflammatory responses in the lung. However, recent demonstration of the ability of CD103+ dendritic cells to induce inflammatory responses starkly contrasts with their classically described role as regulatory cells. These discrepancies may be attributable to the lack of current information on the importance of CD103 expression and modulation on these cells during inflammatory episodes.MethodsTo verify the importance of CD103 expression in the regulation of hypersensitivity pneumonitis, wild-type and Cd103-/- mice were exposed intranasally to S. rectivirgula and airway inflammation was quantified. Surface expression of CD103 in response to S. rectivirgula exposure was studied and cell transfers were used to determine the relative importance of CD103 expression on dendritic cells and T cells in regulating the inflammation in hypersensitivity pneumonitis.ResultsCd103-/- mice developed an exacerbated inflammatory response as early as 18h following S. rectivirgula exposure. CD103 expression on dendritic cells was downregulated quickly following S. rectivirgula exposure, and cell transfers demonstrated that CD103 expression on dendritic cells specifically (and not T cells) regulates the onset and severity of this response.ConclusionAll in all, we demonstrate that CD103 expression by dendritic cells, but not T cells, is crucial for homeostasis maintenance and the regulation of the TH17 airway inflammatory response in hypersensitivity pneumonitis.

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“…In a murine model, abatacept (ABA) significantly reduced fibrogenic marker levels, T-cell proliferation, and M1/M2 macrophage infiltration in the lungs of Fra-2 mouse model, characterized by ILD and pulmonary vascular remodeling leading to pulmonary hypertension [132]. Moreover, ABA improved ILD, significantly reducing the lung density on chest HRCT and fibrosis histological score [133].…”

Section: Abataceptmentioning

confidence: 99%

Treatment of Rheumatoid Arthritis-Associated Interstitial Lung Disease: Lights and Shadows

Cassone

Manfredi

Vacchi

et al. 2020

JCM

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Rheumatoid arthritis (RA) is a chronic and systemic inflammatory disease affecting 0.5–1% of the population worldwide. Interstitial lung disease (ILD) is a serious pulmonary complication of RA and it is responsible for 10–20% of mortality, with a mean survival of 5–8 years. However, nowadays there are no therapeutic recommendations for the treatment of RA-ILD. Therapeutic options for RA-ILD are complicated by the possible pulmonary toxicity of many disease modifying anti-rheumatic drugs (DMARDs) and by their unclear efficacy on pulmonary disease. Therefore, joint and lung involvement should be evaluated independently of each other for treatment purposes. On the other hand, some similarities between RA-ILD and idiopathic pulmonary fibrosis and the results of the recent INBIULD trial suggest a possible future role for antifibrotic agents. From this perspective, we review the current literature describing the pulmonary effects of drugs (immunosuppressants, conventional, biological and target synthetic DMARDs and antifibrotic agents) in patients with RA and ILD. In addition, we suggest a framework for the management of RA-ILD patients and outline a research agenda to fill the gaps in knowledge about this challenging patient cohort.

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The effect of CTLA-4Ig, a CD28/B7 antagonist, on the lung inflammation and T cell subset profile during murine hypersensitivity pneumonitis

Cited by 17 publications

References 36 publications

Treatment with abatacept prevents experimental dermal fibrosis and induces regression of established inflammation-driven fibrosis

Treatment with abatacept prevents experimental dermal fibrosis and induces regression of established inflammation-driven fibrosis

Hypersensitivity pneumonitis onset and severity is regulated by CD103 dendritic cell expression

Treatment of Rheumatoid Arthritis-Associated Interstitial Lung Disease: Lights and Shadows

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