Tuesday, 12 July 2022

Malevolent Designer News - Another Piece of Malevolent Design, or a Stupid Mindless Blunder?

UT Southwestern researchers capture first images of antibody attacking neuron receptor: Newsroom - UT Southwestern, Dallas, Texas

Using cryo-electron microscopy, scientists at the University of Texas Southwestern Medical Center have, for the first time, photographed an antibody attacking a neuron.

Auto-immune diseases, where the body's immune system attacks the body itself, present intelligent [sic] deign creationists with some very special problems, none of which they can never be induced to discuss or explain in ID terms.

For example, a system supposedly designed by an omniscient, omnipotent designer simply should not go rogue and turn on the person it is designed to defend, unless of course, that was the intention all along and is a feature of the design! But then again, why doesn't this always work so everyone has these auto-immune diseases, and why are those who suffer from them usually children, apparently randomly selected for this piece of nastiness?

Binding of patient-derived autoimmune antibodies to the GABAA receptor illuminated by cryo-electron microscopy.


From the UTWestern News release:
Autoimmune encephalitis
Autoimmune encephalitis occurs when antibodies or T-cells go rogue and attack the brain. In this study, UTSW researchers and colleagues from Berlin used cryo-electron microscopy to determine the atomic structures of autoantibodies bound to the GABAA receptor. That receptor is an important protein in the brain and a target in autoimmune encephalitis.
Researchers have studied autoimmune diseases – a class of conditions in which the immune system attacks healthy parts of the body – for decades. However, the first autoimmune disease targeting a neuronal receptor protein was discovered just 15 years ago, Dr. Noviello explained. Since then, researchers have reported the existence of a handful of other diseases that fall into this category. These include autoimmune encephalitis, a condition characterized by the sudden onset of severe symptoms including psychosis, seizures, movement disorders, impaired consciousness, and problems with the autonomic nervous system, which controls involuntary bodily functions.

Researchers in Germany recently identified a patient, then 8 years old, whose autoimmune encephalitis appeared to be caused by antibodies that attack the GABAA receptor, a protein that sits on the surface of synapses – specialized structures that connect brain cells. This receptor’s role is to inhibit neuronal firing, balancing the electrical signals prompted by excitatory receptors to maintain healthy signaling between nerve cells.

After confirming that two kinds of antibodies derived from this young patient’s immune cells readily bound to the GABAA receptor, Drs. Noviello, Hibbs, and their colleagues in the Hibbs lab performed cryo-EM – a technique that freezes proteins in place to get high-resolution microscopic images – for each antibody bound to the receptor. UTSW’s cryo-EM facility, opened in 2016 with support from the Cancer Prevention and Research Institute of Texas (CPRIT), provides 3D images of biological molecules up to atomic resolution.

The images show that, both together and separately, the antibodies prevent the GABAA receptor from inhibiting neuronal signaling, causing neurons to become too electrically excited and leading to brain inflammation, cell death, and seizures characteristic of autoimmune encephalitis. Screening for these antibodies could lead to better diagnosis of this condition, said Dr. Noviello; likewise, finding ways to block the interaction between these antibodies and their target could lead to better ways to treat it.
Sadly, the team's research paper published in Cell is behind an expensive paywall but the abstract can be read here. In it the authors say:
Autoantibodies targeting neuronal membrane proteins can cause encephalitis, seizures, and severe behavioral abnormalities. While antibodies for several neuronal targets have been identified, structural details on how they regulate function are unknown. Here we determined cryo-electron microscopy structures of antibodies derived from an encephalitis patient bound to the &gama;-aminobutyric acid type A (GABAA) receptor. These antibodies induced severe encephalitis by directly inhibiting GABAA function, resulting in nervous-system hyperexcitability. The structures reveal mechanisms of GABAA inhibition and pathology. One antibody directly competes with a neurotransmitter and locks the receptor in a resting-like state. The second antibody targets the subunit interface involved in binding benzodiazepines and antagonizes diazepam potentiation. We identify key residues in these antibodies involved in specificity and affinity and confirm structure-based hypotheses for functional effects using electrophysiology.
Clearly, the human immune system comes within what any ID advocate would define as an example of design, which they also argue points to a designer. Unfortunately, the only way to explain this phenomenon in terms of design is either incompetence or malevolence, since a well-designed immune system should not be turning on the person it was designed to protect - unless the designer intended random children to get auto-immune encephalitis and be severely incapacitated or dead.

Perhaps a creationist would like to take this opportunity to explain why we should not regard the designer of an immune system that can end up causing this condition in children as incompetent at best and malevolent at worst, bearing in mind that the Discovery Institute is still insisting that intelligent [sic] design is a valid scientific alternative to the science of evolution that should be taught as such to school children, and not a religious notion.


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