F Rosa Rubicondior: Unintelligent Design - How Scientists Are Overcoming The "Designer's" Incompetence

Wednesday 7 February 2024

Unintelligent Design - How Scientists Are Overcoming The "Designer's" Incompetence

Systemic lupus erythematosus
World-first discovery may enable an effective long-term lupus treatment - Monash University

Readers may recall my recent article on Lupus and why women are nine times more likely to suffer from it than men, because the epigenetic process for switching off genes on their X-chromosome sometimes goes wrong and produces proteins that induce an immune response to their own tissues.

From a creationist perspective, this can only be for one of two reasons: either the designer was incompetent, or this was by design. The choice being either incompetence, or malevolence and misogyny.

Now a team of researchers at Monash University, Clayton, VIC, Australia, have reported success in finding a way to overcome this design defect - which begs the question: if scientists can do it, why couldn't an omnipotent intelligent designer? Could the answer be that the human immune system was not designed by an omnipotent, intelligent designer, but is the result of a mindless, utilitarian process that inevitably produces sub-optimal 'designs' that can't be scrapped and redesigned?

But that is the kind of thought that would cause panic in the mind of most creationists because it would raise the terrible spectre of wondering if they could be wrong.
The Australian team have just published their results, open access, in Nature Communications. They are also explained in a Monash University news release:
Australian researchers have worked out how to fix a defect that causes lupus, and hope their world-first discovery will offer effective long-term treatment.

Published in Nature Communications, the Monash University-led study found a way to reprogram the defective cells of lupus patients with protective molecules from healthy people.

Using human cells, the new treatment restores the protective side of the immune system that prevents autoimmunity, which is when the immune system attacks its own cells. The findings relate to the autoimmune disease lupus, a debilitating disease with no cure and limited treatments.

But researchers hope this new method, developed in test tubes and proven in pre-clinical models, can also be developed for other autoimmune diseases such as diabetes, rheumatoid arthritis, and multiple sclerosis.

Humans all have proteins that the immune system could attack, but this doesn’t happen in healthy people because of special cells called ‘regulatory T cells’ or ‘T-regs’ that protect from autoimmune disease. These are lacking in people who develop lupus and other autoimmune conditions.

Co-senior author Associate Professor Joshua Ooi, who heads Monash University’s Regulatory T Cell Therapies Group based at Monash Health, said the therapeutic effect was achieved by identifying specific protective molecules from healthy people and reprogramming ineffective lupus patient T-regs to restore their ability to switch off unwanted immune responses.

We showed the effectiveness of this approach using human lupus patient cells, both in the test tube and in an experimental model of lupus kidney inflammation. We were able to completely arrest the development of lupus kidney disease, without the use of the usual non-specific and harmful immunosuppressant drugs. It’s like a reset of the abnormal immune system back to a healthy state – kind of like a major software upgrade. That it uses the patient’s own cells is a very special part of this.

Associate Professor Joshua D. Ooi, co-senior author
Centre for Inflammatory Diseases
Department of Medicine
School of Clinical Sciences
Monash University, Clayton, VIC, Australia
About one in 1000 Australians has lupus, and rates are higher in First Nations communities. Nine in 10 people with lupus are female and most develop it aged 15-45.

Co-senior author Professor Eric Morand, who is Dean of Monash University’s Sub Faculty of Clinical & Molecular Medicine and founded the Monash Lupus Clinic, described the treatment’s effectiveness as “profound” and a “game-changer”.

Study patients are managed at Monash Health, where Professor Morand is Director of Rheumatology. He said the research team was now designing clinical trials expected to start in 2026 to investigate whether this method was a long-term cure for people with lupus.

The ability to target, specifically, the disease-causing immune defect, without the need to suppress the entire immune system, is a game-changer. Even if the effects are only medium term, we are confident the treatment can be easily repeated as needed.

Professor Eric F. Morand, co-senior author
Centre for Inflammatory Diseases
Department of Medicine
School of Clinical Sciences
Monash University, Clayton, VIC, Australia
Associate Professor Ooi previously discovered that a lack of specific T-regs to stop the immune system from targeting the body can lead to autoimmune disease. The new treatment would involve taking blood cells from the lupus patient, modifying them in the lab to restore this protective effect, then giving them back.

“This project relied on the generous involvement of patients, which enabled us to use human lupus cells every step of the way,” Associate Professor Ooi said. “This allows us to work as close to the human disease as possible in the lab.

“This is a unique characteristic of Monash University — state-of-the-art research labs side-by-side with clinicians and patients, in this case at Monash Health.”

Co-first authors Peter Eggenhuizen, a PhD candidate and Research Fellow with the Centre for Inflammatory Disease Monash University, and Dr Rachel Cheong, former PhD candidate at the Centre for Inflammatory Disease Monash University, are confident the new method can be developed for up to 100 other autoimmune diseases such as diabetes, rheumatoid arthritis, multiple sclerosis, Sjögren's syndrome, scleroderma, and myasthenia gravis.

This breakthrough offers huge hope not only in lupus but across the spectrum of autoimmune diseases. There is a huge range of autoimmune diseases that could be targeted with this approach.

Peter J. Eggenhuizen, co-first author
Centre for Inflammatory Diseases
Department of Medicine
School of Clinical Sciences
Monash University, Clayton, VIC, Australia
Added Dr Cheong: “The great thing is that because the treatment is very specific, it doesn’t harm the rest of the immune system. However, this means that the treatment needs to be carefully developed disease-by-disease, as each one is distinct.”

This research was supported by multiple national and international agencies, including the New-York headquartered Lupus Research Alliance, and was part of a body of work that won Professor Morand and Associate Professor Ooi the 2022 Victoria Prize for Science and Innovation in Life Sciences.

Case study - Vu Nguyen
Vu Nguyen, 39

Vu Nguyen, 39, was diagnosed with Lupus in 1995 aged nine after she developed swelling and pain in her joints. Almost 30 years later, Vu has experienced a range of symptoms, kidney biopsies and hospital stays. She had a stroke when she was 22 and now has epilepsy, which is secondary to lupus.

It took many years to stabilise Vu’s condition, which inspired her to establish Lupus Victoria. A Masters of Marketing graduate, Vu is completing psychological science post-graduate qualifications so she can counsel those who have the disease.

My main symptoms are now bad functioning kidneys and my epilepsy. With Lupus, it always changes. I'm currently in remission but I've had a lot of ups and downs with this disease. I think the lupus has made my body more prone to having the stroke and subsequent epilepsy. I am good at the moment. It's just the epilepsy that's currently attacking my body.

This new treatment will really help people living with lupus; if the treatment was around 30 years ago it would have made a real difference for me. It could really cut down the many different types of medicines we take. With this procedure, we could possibly need just one treatment.

This is how the team describe their findings in Nature Communications:

Antigen-specific regulatory T cells (Tregs) suppress pathogenic autoreactivity and are potential therapeutic candidates for autoimmune diseases such as systemic lupus erythematosus (SLE). Lupus nephritis is associated with autoreactivity to the Smith (Sm) autoantigen and the human leucocyte antigen (HLA)-DR15 haplotype; hence, we investigated the potential of Sm-specific Tregs (Sm-Tregs) to suppress disease. Here we identify a HLA-DR15 restricted immunodominant Sm T cell epitope using biophysical affinity binding assays, then identify high-affinity Sm-specific T cell receptors (TCRs) using high-throughput single-cell sequencing. Using lentiviral vectors, we transduce our lead Sm-specific TCR into Tregs derived from patients with SLE who are anti-Sm and HLA-DR15 positive. Compared with polyclonal mock-transduced Tregs, Sm-Tregs potently suppress Sm-specific pro-inflammatory responses in vitro and suppress disease progression in a humanized mouse model of lupus nephritis. These results show that Sm-Tregs are a promising therapy for SLE.


Regulatory T cells (Tregs) are essential for maintaining immune homeostasis by acting in a variety of ways on different immune cell types (Fig. 1). Decreased Treg numbers and/or defective Treg function have been implicated in the development of autoimmune diseases1, such as systemic lupus erythematosus (SLE)2,3. Treg-based therapeutic approaches, such as expansion of polyclonal4 or antigen-specific Tregs5, are increasingly being explored, and antigen-specific Tregs, in particular, have been shown to suppress pathogenic autoreactivity6. .
  Fig. 1: Sm-TCR Treg mechanisms of action
Sm-TCR Tregs act through a variety of mechanisms to suppress autoreactivity and restore immune tolerance. Tregs can suppress autoreactive B cells and autoantibody production, suppress pathogenic T cells, tolerize antigen-presenting cells such as dendritic cells, and can directly lyse inflammatory cells. TCR transduction of a Sm-specific TCR renders the Treg more potent in its ability to specifically suppress lupus nephritis. Created with BioRender.com.
Lupus nephritis (LN), a severe manifestation of SLE, is an important contributor to disease related morbidity and mortality7. The presence of LN is strongly associated with autoreactivity to the Smith (Sm) autoantigen8, which is in turn strongly associated with carriage of the human leukocyte antigen (HLA) haplotypes DRB1*15:01 (DR15) and DRB1*03:01 (DR3)9,10,11. Whether these associations are causal, and afford a therapeutic opportunity, can be explored through the design of an Sm antigen-specific Treg. Here, we develop a platform to establish autoantigen-specific Treg-cell-based therapy for autoimmune diseases (Fig. 2). In LN, we identify Sm HLA-DR15 restricted CD4+ T-cell epitopes and highly reactive TCRs of the most immunogenic epitopes, create antigen-specific Tregs for the Sm autoantigen (Sm-Tregs), and evaluate the capacity of Sm-Tregs to suppress disease activity in vitro and in a humanized mouse model of lupus nephritis.
  Fig. 2: Pipeline for the development of antigen-specific Tregs for autoimmune disease.
To develop an antigen-specific Treg targeting an autoimmune disease a 6-step process is undertaken. In the case of lupus nephritis, Sm-Tregs are developed as follows. (1) The immunogenic autoimmune epitope, the Smith antigen (Sm), in the context of human leukocyte antigen (HLA)-DR15 is identified. (2) T-cell receptors (TCRs) are identified specific for Sm. (3) Candidate TCRs are screened for high expression, specificity and reactivity and a lead Sm TCR is chosen. (4) Lead Sm TCR is validated for its functional responses on Tregs in vitro and in vivo. (5) The pre-clinical data package is sent for regulatory approval and good manufacturing practice (GMP) cell manufacture commences. (6) Sm-Tregs are tested in human clinical trials for safety and efficacy. Created with BioRender.com.
If scientists can produce a cure for lupus, then why couldn't creationism's allegedly intelligent designer have prevented it in the first place, by designing an immune system that doesn't go wrong and turn on us, or, if that wasn't within its capabilities, why didn't it design the cure? The reason of course is that the human immune system was 'designed' by a mindless, unintelligent system that frequently produces sub-optimal systems that mostly work, most of the time, and so are better than nothing. This is how we can tell that no intelligence, malevolent or benevolent, was involved in their design.


The Unintelligent Designer: Refuting The Intelligent Design Hoax

ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.

Available in Hardcover, Paperback or ebook for Kindle


The Malevolent Designer: Why Nature's God is Not Good

This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.

Illustrated by Catherine Webber-Hounslow.

Available in Hardcover, Paperback or ebook for Kindle


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