Rosa Rubicondior: Unintelligent Design - How The Badly-Designed Immune System Destroys Lungs

Sunday, 30 March 2025

Unintelligent Design

How The Badly-Designed Immune System Destroys Lungs

Scientists Discover Immune Cell Networks Driving Deadly Lung Disease | Rutgers University

Autoimmune conditions and allergies provide strong evidence for evolution over intelligent design by highlighting the imperfections and trade-offs inherent in the immune system. These disorders demonstrate how a system shaped by natural selection can prioritize short-term survival at the expense of long-term health, leading to vulnerabilities that are difficult to reconcile with the concept of a perfect designer.

Autoimmune diseases occur when the immune system mistakenly attacks the body’s own tissues. Examples include rheumatoid arthritis, lupus, multiple sclerosis, and type 1 diabetes.

The immune system must strike a delicate balance: it must be reactive enough to fight infections but tolerant enough to avoid attacking the body’s own cells. Evolution has shaped this balance, but it is imperfect. A hyperactive immune system, while better at combating infections, increases the risk of autoimmune diseases.

The Body of Evidence: How the Human Body Refutes Intelligent Design pp. 129-130

Now it's beginning to look like we must include the fatal lung disease known as idiopathic pulmonary fibrosis (IPF) to the long list of autoimmune conditions that stem directly from the facts that the immune system evolved and was not intelligently designed.

The very existence of the immune system should prompt creationists to reconsider several basic beliefs and especially claims made by leading proponents, such as Michael J. Behe. Behe suggests that pathogens and the diseases they cause result from 'genetic entropy', a degradation enabled by biblical 'Sin', which supposedly causes genomes to 'devolve', thus creating parasites and pathogens. Other creationists suggest an alternative viewpoint, attributing the existence of parasites and diseases to an evil designer, such as Satan - a claim which is regarded as blasphemous by fundamentalists for whom it is doctrine that there is only one creative entity - God.

In contrast, William A. Dembski argues that any 'complex specified information' (CSI) within the genome must originate from an intelligent designer, typically inferred — though seldom explicitly acknowledged by prominent creationists — as the God described in the Bible or the Qur'an. The genes that enable parasites to evade our immune defences are clear examples of what Dembski would term CSI, whereas Behe regards these genes as 'devolved' from an initially perfect creation.

However, neither Behe nor Dembski adequately addresses the question of who or what designed the immune system itself. Was it the same designer responsible for Dembski's complex specified information, or was it Behe's designer of an initial, perfect creation? If we consider Dembski's argument, it raises a critical question: where is the intelligence in designing an immune system to protect organisms against pathogens created by the very same designer? Regarding Behe's perspective, if the immune system were part of the initial perfect design, why would the designer anticipate 'The Fall' and its consequences unless it was intentionally planned? Alternatively, did all organisms possessing immune defences receive an upgrade after 'The Fall', indicating a supposedly omniscient deity initially failed to foresee the need for such protection? This then raises the question, is the designer either not omniscient or not competent, or did it plan for the 'Fall' and the suffering caused by parasites all along?

Not only are there these gaping flaws in creationism's attempts to account for the immune system within their own theology, including its failure to protect us and its propensity to attack us because the delicate balance referred to above is not robust enough or sensitive enough. The fact is that a perfectly designed immune system should make much of medical science redundant. However, the evidence continues to accumulate that the immune system, like the rest of biology is not the result of intelligent design but of an evolutionary process with all its inherent faults, constraints and inevitable suboptimal compromises.

Evidence strongly supporting the theory that IPF is the result of an autoimmune response by an over-sensitive immune system has been provided by a team of researchers led by Rutgers University, New Jersey, USA. Their findings are being published in the European Respiratory Journal and are described in Rutgers Today:

Tell me all about Idiopathic Pulmonary Fibrosis that recent research suggests is an autoimmune disease.

Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive lung disease characterized by the thickening and scarring (fibrosis) of lung tissue, leading to a decline in respiratory function. The term "idiopathic" indicates that the exact cause remains unknown. However, recent research suggests potential autoimmune components in its pathogenesis.

Autoimmune Aspects in IPF:

Autoantibodies: Studies have identified the presence of specific autoantibodies in IPF patients. For instance, anti-periplakin (PPL) autoantibodies were detected in both the bloodstream and bronchoalveolar lavage fluid of nearly half of the IPF patients studied. This finding suggests an autoimmune response targeting lung tissue components. Reference.
Immune Cell Infiltration: Comparative analyses between IPF and other autoimmune-related lung diseases have revealed significant lymphocytic infiltrations in the lung tissues of IPF patients. These infiltrations are indicative of an immune-mediated process contributing to lung fibrosis. Reference.
Predictive Autoimmune Signatures: Advanced proteomic analyses have uncovered specific autoimmune signatures in IPF patients. Notably, autoantibodies against thrombospondin-1 (THBS1) have been associated with reduced transplant-free survival, highlighting their potential role as predictive biomarkers for disease progression. Reference.
Implications for Treatment:

The recognition of autoimmune mechanisms in IPF opens avenues for novel therapeutic strategies. Traditional antifibrotic therapies may be complemented by treatments targeting autoimmune pathways, potentially improving patient outcomes. Ongoing research is focused on understanding these mechanisms to develop more effective interventions.

Conclusion:

While IPF has traditionally been considered a disease of unknown origin, emerging evidence points to autoimmune processes playing a significant role in its development and progression. Further research is essential to fully elucidate these mechanisms and translate findings into targeted therapies.

ChatGPT4.5 [Response to user request]
Retrieved from https://chatgpt.com/

Information Continually updated

Scientists Discover Immune Cell Networks Driving Deadly Lung Disease
Rutgers Health researchers have discovered that networks of misplaced immune cells drive an aggressive lung disease, potentially opening a path to new treatments for a condition that kills 80% of patients within a decade.
Idiopathic pulmonary fibrosis (IPF) scars lung tissue and makes breathing increasingly difficult until patients can’t get enough oxygen. Available drugs provide minimal benefit. Lung transplantation works for some patients, but transplants have a 50% five-year mortality rate.

The study in the European Respiratory Journal used advanced spatial mapping techniques to compare healthy lung tissues and tissues from patients with fatal IPF. The researchers discovered that disease-scarred lung tissue abounds in plasma cells – specialized immune cells that typically reside in bone marrow and produce antibodies.

What we found most striking in this study is that all the fibrotic regions of IPF patients' lungs are covered by antibody-producing plasma cells. In normal lungs, there are almost no plasma cells. But in IPF patients, the lungs are full of them.

Assistant Professor, Dr. Qi Yang, joint senior author
Child Health Institute of New Jersey
Rutgers Robert Wood Johnson Medical School
New Brunswick, NJ, USA.

The researchers identified previously unknown cellular networks orchestrating this abnormal immune response. They discovered novel mural cells wrapping around blood vessels and producing signal proteins that organize immune responses. They also found unique fibroblasts secreting a protein that attracts plasma cells to damaged areas.

This particular type of fibroblast has never been described before. People have shown that fibroblasts are the cell types responsible for scarring – in the skin, the lungs and the brain – but this particular type of fibroblast seems unique to the lung.

Reynold Panettieri, joint-senior and co-corresponding author
Rutgers Institute for Translational Medicine and Science
Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA.

Having found the plasma cells in lung tissue taken from people who died of IPF, the team began using live mice to see if reducing plasma in the lungs slowed disease formation. This work demonstrated that blocking signaling pathways reduced plasma cell accumulation and alleviated lung scarring. Targeting these same signaling pathways may thus prove an effective disease treatment in humans, the researchers said.

The research is particularly promising because drugs targeting plasma cells already exist. Medications used to treat multiple myeloma, a plasma cell cancer, could potentially be repurposed to treat IPF.

If the plasma cells are really making the bad antibodies, I assume we may have to get rid of them, otherwise, patients will keep making these antibodies that drive the disease.

Assistant Professor, Dr. Qi Yang.

Previous studies have shown that IPF patients have heightened antibody responses and elevated lung antibody levels. The new research explains the origin of these antibodies and reveals how abnormal antibody-producing cells accumulate in the lungs.

The researchers said the antibodies may drive tissue damage through several mechanisms. Their data suggest that antibody-antigen complexes stimulate the production of transforming growth factor-beta from pulmonary macrophages, thus promoting fibrosis.

Now that we have a target, a cell, a unique cell that Dr. Yang has identified and phenotyped, we're optimistic that we could affect that cell and not other fibroblasts that are important in normal injury repair response.

Reynold Panettieri.

For patients with IPF, the findings offer hope of new treatments for a debilitating condition with limited therapeutic options. The disease typically affects men over 60 years of age, with most patients dying within five years of diagnosis.

The next steps for the research team include determining whether the plasma cells are producing autoantibodies against healthy tissues and further investigating how fibroblasts and mural cells develop their abnormal properties in IPF.

Our research suggests that IPF might have a strong autoimmune link.

Assistant Professor, Dr. Qi Yang.

The study represents a collaborative effort between the Child Health Institute of New Jersey and the Rutgers Institute for Translational Medicine and Science, combining mouse model research with analysis of human lung tissue from end-stage IPF patients.

Abstract

Background
Idiopathic pulmonary fibrosis (IPF) is characterized by significant, but poorly understood immune and antibody responses. This study examines the spatial transcriptomes and microenvironmental niches of antibody-producing plasma cells and tertiary lymphoid structures (TLS) in IPF lungs, and the molecular pathways influencing antibody accumulation and pulmonary fibrosis.

Methods
Explant lung tissues from IPF patients and control normal lungs were used for spatial transcriptome assays and validating RNA-scope and immunofluorescence assays. Fibroblasts derived from IPF and control lungs were examined for their capability to attract plasma cells. Neutralizing antibodies were administered to investigate molecules affecting pulmonary plasma cell accumulation and fibrosis in bleomycin-treated mice.

Results
Human IPF lungs exhibited a remarkably widespread distribution of plasma cells and local antibodies in the fibrotic regions, disseminating from plasma cell-generating TLS. Novel mural cells wrapped the vessels in TLS regions, expressing CCR7 ligands that attracted T cells into TLS to promote plasma cell generation. Distinct IPF-associated fibroblasts further secreted CXCL12, providing an extramedullary niche to foster the dissemination and accumulation of plasma cells in the fibrotic regions. Neutralization of CCR7 ligands or CXCL12 reduced plasma cell and local antibody accumulation in the lungs of bleomycin-treated mice, leading to reduced TGFβ concentrations and alleviated pulmonary fibrosis.

Conclusions
Plasma cells and local antibodies are widely distributed in the fibrotic regions of IPF lungs. Distinct subsets of IPF-associated mural cells and fibroblasts promote pathological plasma cell and antibody accumulation. These findings have potential implications for strategies aimed at targeting immune and antibody responses to combat IPF.

Footnotes

This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article.

Yang, Zhi; Cao, Gaoyuan; Tan, Xiaosheng; Orfanos, Sarah; Jude, Joseph; Barbet, Gaetan; An, Steven S.; Jiang, Dianhua; Panettieri, Reynold A.; Yang, Qi
Distinct mural cells and fibroblasts promote pathogenic plasma cell accumulation in idiopathic pulmonary fibrosis
European Respiratory Journal (2025) 2401114; DOI: 10.1183/13993003.01114-2024

© 2025 European Respiratory Society.
Reprinted under the terms of s60 of the Copyright, Designs and Patents Act 1988.

If confirmed, the evidence linking idiopathic pulmonary fibrosis to autoimmune processes would strongly argue against the intelligent design hypothesis regarding the human immune system, instead supporting evolutionary explanations. An immune system that mistakenly attacks the body's own tissues exemplifies not intelligent planning, but rather inherent flaws consistent with evolutionary development through trial-and-error. Advocates of intelligent design must consider whether they wish to persist in defending a designer whose creations would suggest incompetence or even malevolence, or acknowledge that evolutionary theory offers a realistic, coherent, and evidence-based explanation for diseases, parasites, and other suboptimal biological systems, including our overly complex yet frequently error-prone immune defences.

Advertisement

Amazon