Publications by authors named "Carlos Zamora-Atenza"

Immune-related adverse events (irAEs) are unpredictable autoimmune-like toxicities induced by immune checkpoint inhibitors (ICI). irAEs are a consequence of a breakdown in self-tolerance. ICIs can induce autoantibody formation, and the presence of antinuclear autoantibodies (ANAs) has been reported in patients who developed irAEs.

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Pulmonary fibrosis involves various types of immune cells and soluble mediators, including TGF-β and IL-35, a recently identified heterodimeric cytokine that belongs to the IL-12 cytokine family. However, the effect of regulatory IL-35 may play an important role in fibrotic diseases. The aim of this paper is to explore the immunoregulatory role of IL-35 in the development of fibrosis in interstitial lung disease (ILD).

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Article Synopsis
  • - The study investigates the role of tumor PD-L1 expression as a biomarker in predicting the effectiveness of PD-(L)1 blockade treatments for advanced non-small cell lung cancer (NSCLC) patients, noting that responses can occur regardless of tumor PD-L1 levels.
  • - Researchers analyzed blood samples from 119 NSCLC patients, checking for various PD-L1 expressions on immune cells, platelets, and in plasma, alongside tumor PD-L1 levels, to better correlate these factors with treatment efficacy.
  • - Findings indicate that incorporating both circulating and tumor PD-L1 data can significantly predict patient outcomes and may guide treatment decisions for those eligible for PD-(L)1 blockade therapy.
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Psoriasis is currently considered to be an immune-mediated disease whose patho-mechanisms involve platelet activation, which seems to correlate with the activity of the disease. Platelet activation is associated with the formation of platelet-lymphocyte complexes (PLyC), although their significance remains unknown. Moreover, biological treatments that target tumor necrosis factor-α (TNF-α) reduce platelet activation.

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Introduction: Adalimumab is a fully human anti-tumor necrosis factor α (anti-TNFα) monoclonal antibody that specifically blocks the interaction of TNFα with its receptors. It binds both soluble and transmembrane TNFα. We hypothesized that blocking these TNFα signals regulates the altered TNFα production in rheumatoid arthritis (RA) patients.

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The exact function of interleukin-19 (IL-19) on immune response is poorly understood. In mice, IL-19 up-regulates TNFα and IL-6 expression and its deficiency increases susceptibility to DSS-induced colitis. In humans, IL-19 favors a Th2 response and is elevated in several diseases.

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