Celiac Disease and Its Impact on the Immune System

Understand how celiac disease affects the immune system and explore key insights about managing this condition.

Abstract

In my years of clinical practice, I have seen countless individuals struggling with unexplained symptoms ranging from digestive distress and skin issues to neurological problems and chronic fatigue. A significant portion of these cases can be traced back to the complex interaction between the food we eat, particularly gluten, and our immune system. This educational post will take you on a journey deep into the physiology of gluten sensitivity and celiac disease, two conditions that are often misunderstood and mismanaged. We will explore the critical differences between non-celiac gluten sensitivity (NCGS), an innate immune response, and celiac disease, a permanent adaptive autoimmune condition. I will detail the molecular mechanisms behind “leaky gut” or intestinal hyperpermeability, explaining the roles of proteins like gliadin and zonulin, and how the enzyme tissue transglutaminase (TTG) becomes a target for autoimmune attack. We will discuss appropriate diagnostic testing, including the need for a gluten challenge for accurate results, and why concepts like molecular mimicry, cross-reactivity, and the threshold effect are essential to understanding why these conditions can suddenly manifest later in life. This post will also highlight our unique multidisciplinary approach at Injury Medical Clinic, where I, as a Doctor of Chiropractic with extensive training in functional medicine, work closely with our esteemed Medical Director, Dr. Maria Guadalupe Cardenas, MD. Dr. Cardenas, a Board-Certified Internist with over 40 years of experience, provides invaluable medical oversight, allowing us to create a truly integrative and comprehensive care model that addresses the root cause of chronic illness. Our goal is to empower you with the knowledge to understand your body and provide a clear path toward healing and long-term wellness.

Our Integrative Approach to Complex Health Issues

Before we delve into the intricate science of gluten-related disorders, I believe you must understand the philosophy and structure of our practice. At Injury Medical Clinic PA, in El Paso, Texas, we have cultivated a unique healthcare environment built on collaboration and a shared commitment to patient-centered care. I am Dr. Alex Jimenez, and my journey in healthcare has led me to accumulate a diverse set of credentials, including Doctor of Chiropractic (DC), Advanced Practice Registered Nurse (APRN), Family Nurse Practitioner-Board Certified (FNP-BC), and certifications in Functional Medicine (CFMP, IFMCP), among others. This background allows me to view health through multiple lenses, from the structural integrity of the musculoskeletal system to the biochemical complexities of cellular function.

However, our clinic’s strength lies in our multidisciplinary team. I have the honor of working alongside Dr. Maria Guadalupe Cardenas, MD, our Medical Director and Collaborative Physician. Dr. Cardenas is a highly respected, Board-Certified Internist with an impressive career spanning over four decades. Her profound expertise in internal medicine provides the essential medical oversight and diagnostic acumen that anchors our practice. This collaborative model, where a Doctor of Chiropractic works hand in hand with a Medical Doctor, is a cornerstone of modern integrative healthcare, particularly in complex chronic illness and personal injury rehabilitation.

This partnership allows us to offer a spectrum of care that no single practitioner could. When a patient presents with symptoms, our team can evaluate them from both musculoskeletal and systemic medical perspectives. My role often involves using chiropractic adjustments to optimize nervous system function and structural alignment, which is foundational to health. At the same time, Dr. Cardenas provides the medical diagnosis, oversees necessary lab work and prescriptions, and ensures all treatments are medically sound and safe. Together, with our team of rehabilitation specialists and functional medicine experts, we create a cohesive treatment plan that addresses the patient as a whole person, not just a collection of symptoms. This integrated approach is particularly powerful when dealing with conditions like gluten sensitivity and celiac disease, where the manifestations are systemic and require a multifaceted strategy for recovery.

The Critical Distinction: Celiac Disease vs. Non-Celiac Gluten Sensitivity

In the world of conventional medicine, there has often been a tendency to group all adverse reactions to gluten under one umbrella, or worse, to dismiss the symptoms if a patient tests negative for celiac disease. From my clinical experience and a deep dive into the research, I can tell you this is a profound oversimplification with serious consequences for patient health. It is imperative to understand that celiac disease and non-celiac gluten sensitivity (NCGS) are two fundamentally different biological processes.

Celiac Disease: An Adaptive Autoimmune Attack

Celiac disease is not a simple intolerance or allergy; it is a serious, genetically predisposed autoimmune disorder. This means it involves the adaptive immune system—the highly specific and intelligent branch of your immunity that develops memory. When someone with celiac disease consumes gluten, the body launches a precise and targeted attack, not just against the gluten protein, but against its own tissues. This response is permanent. Once the switch for celiac autoimmunity is flipped on, it cannot be flipped off.

In this case, the immune system creates specific antibodies, primarily Immunoglobulin G (IgG) and Immunoglobulin A (IgA), directed against an enzyme in our own body called tissue transglutaminase (TTG). As we will explore in detail later, this enzyme binds to a component of gluten, and the immune system mistakenly identifies the entire complex—and therefore our own tissue—as a dangerous invader. The long-term consequences of this continuous autoimmune assault, triggered by ongoing gluten and, often, dairy consumption, are devastating. It progressively destroys the intestinal lining, which in turn causes severe nutrient malabsorption. This malabsorption is the gateway to a cascade of systemic problems, including osteoporosis (due to poor calcium and vitamin D absorption), a wide range of neurological disorders (from brain fog and migraines to ataxia and neuropathy), and an increased risk of cardiovascular damage as chronic inflammation takes its toll on the entire body. The mechanism is the slow, relentless killing of the intestinal villi, the tiny, finger-like projections in the small intestine responsible for absorbing the nutrients from our food.

Non-Celiac Gluten Sensitivity (NCGS): An Innate Immune Irritation

In stark contrast, non-celiac gluten sensitivity (NCGS) is primarily an innate immune reaction. The innate system is our body’s first line of defense. It’s less specific and more generalized than the adaptive system. Think of it as the bouncer at the door, reacting to anything that looks suspicious, rather than the detective that builds a specific case file (which is what the adaptive immune system does).

In NCGS, the body is not launching a self-destructive autoimmune attack. Instead, it is reacting to the structural components of the wheat plant itself. The irritation can be caused by:

• Gluten Proteins: The sheer complexity and size of certain gluten proteins can be inherently difficult to digest and inflammatory for some individuals.
• Amylase-Trypsin Inhibitors (ATIs): These are non-gluten proteins found in modern wheat that are potent activators of the innate immune system. Research has shown they can directly trigger an inflammatory response in the gut (Zevallos et al., 2017).
• Fructans: These are a type of carbohydrate known as a FODMAP (Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols). Fructans are poorly absorbed in the small intestine and travel to the large intestine, where gut bacteria rapidly ferment them. This fermentation process produces gas, leading to bloating, pain, and changes in bowel habits—symptoms that heavily overlap with both NCGS and Irritable Bowel Syndrome (IBS).

While the symptoms of NCGS—such as bloating, abdominal pain, brain fog, headaches, and fatigue—can be incredibly unpleasant and severely impact one’s quality of life, there is a crucial difference: NCGS does not cause the villous atrophy, or the killing of the intestinal villi, that characterizes celiac disease. The reaction is irritation and inflammation, not targeted autoimmune destruction of the gut lining.

The Diagnostic Dilemma: Getting the Right Test at the Right Time

This distinction between celiac and NCGS brings us to a critical point: accurate diagnosis. The gold standard screening test for celiac disease is a blood test that measures antibodies against tissue transglutaminase, specifically the TTG-IgA test. However, this test has a major caveat that many clinical settings tragically overlook.

For your body to produce the antibodies that this test measures, it must be actively exposed to the trigger—in this case, gluten. If you have already removed gluten from your diet in an attempt to feel better, your immune system will eventually stop producing these specific celiac-related antibodies. If you then go for a TTG-IgA test, the result will likely be a false negative. The test will come back normal, and you may be told, “You don’t have celiac disease, so gluten is not your problem.” This is a critical piece of misinformation.

To ensure an accurate celiac disease test, a patient must consume a significant amount of gluten daily (about four slices of bread) for at least four to six weeks before the blood draw. This is known as a “gluten challenge.” If you are already gluten-free, this prospect can be daunting, as it means deliberately making yourself sick. However, without it, the primary screening test for celiac disease is essentially worthless. I have this conversation with my patients every day, explaining the “why” behind this necessary, albeit difficult, step. It’s a prime example of where our integrative team, with Dr. Cardenas providing medical oversight for the testing protocol, can guide patients safely through this complex diagnostic process.

The Molecular Cascade of Leaky Gut and Autoimmunity

Now, let’s take a microscopic journey into the gut to understand exactly what happens when gluten enters the system of a susceptible individual. This process is at the heart of both celiac disease and many other autoimmune and inflammatory conditions.

The Small Intestine: A Delicate and Intelligent Filter

Imagine your small intestine not as a simple pipe, but as an incredibly sophisticated, intelligent filter. The lining of this tube, known as the intestinal epithelium, is only one cell layer thick. It is one of the most delicate yet vital barriers in the entire human body. Its job is to perform a miraculous task: selectively absorb beneficial nutrients from the food we eat—vitamins, minerals, amino acids, fatty acids—while preventing a toxic soup of undigested food particles, bacteria, viruses, and toxins from entering our bloodstream.

Tight junctions are the gatekeepers of this barrier. You can picture these as molecular “spot welds” or a form of biological glue that holds the intestinal cells (enterocytes) tightly together. When these tight junctions are healthy and secure, the barrier is intact, and only properly digested, single-molecule nutrients can pass through into the circulation.

The Role of Gliadin and the Discovery of Zonulin

When we eat wheat, rye, or barley, we introduce gluten, which is a composite of two main proteins: gliadin and glutenin. For genetically susceptible individuals, gliadin is the primary troublemaker. When gliadin fragments reach the intestinal wall, they trigger a specific, well-documented reaction.

Pioneering research by Dr. Alessio Fasano and his team at Harvard University uncovered the key to this process: a protein called zonulin (Fasano, 2011). Dr. Fasano discovered that gliadin is a potent trigger for the release of zonulin in all humans, not just those with celiac disease. Zonulin modulates tight-junction permeability. In essence, zonulin is the key that unlocks the intestinal barrier.

When gliadin prompts the gut to release large amounts of zonulin, this protein goes to work, literally shredding the tight junctions. The secure, impermeable barrier is compromised. The gates are now wide open. In functional medicine, we call this intestinal hyperpermeability, or more commonly, “leaky gut.”

With the barrier breached, a flood of substances that should have remained safely contained within the intestine now “puke” into the bloodstream. This includes:

• Undigested food proteins (like gliadin itself)
• Lipopolysaccharides (LPS), which are inflammatory components of bacterial cell walls
• Environmental toxins
• Metabolic waste products

This influx of foreign material into the sterile bloodstream triggers a massive, systemic immune alarm. This is the foundational event that can lead to a host of chronic diseases.

The Autoimmune Trigger: Tissue Transglutaminase (TTG)

Once the offending protein, gliadin, leaks into the bloodstream, the next critical step in celiac disease development occurs. The body tries to deal with this foreign invader. An enzyme called tissue transglutaminase (TTG), found throughout the body, attempts to “tag,” or deamidate, the gliadin molecule, modifying it to make it easier for the immune system to recognize and clear.

However, this process creates a new, hybrid molecule: a TTG-gliadin complex. Herein lies the tragic mistake of autoimmunity. The immune system’s surveillance cells, specifically the antigen-presenting cells, see this complex as a unified threat. They present it to the adaptive immune system, which then dutifully creates antibodies to destroy it. The problem is that, in its zeal, the immune system can no longer distinguish between foreign gliadin and the body’s own TTG enzyme.

It begins to produce IgG and IgA antibodies not just against the TTG-gliadin complex, but against TTG itself. This is the hallmark of celiac disease. Your immune system has been programmed to attack a vital part of your own cellular machinery.

And where is tissue transglutaminase found? In high concentrations in three key areas:

1. The Intestinal Villi: This is why the primary site of damage in celiac disease is the gut. Antibodies attack TTG within the villi, leading to inflammation, flattening (villous atrophy), and a catastrophic loss of absorptive capacity.
2. The Endothelium: This is the delicate, one-cell-thick lining of all our blood vessels. Autoimmune attacks here contribute to systemic inflammation and cardiovascular complications.
3. The Skin: TTG is also present in the skin’s dermal papillae. This explains a particularly agonizing manifestation of celiac disease known as dermatitis herpetiformis (DH).

When the Battleground Spreads: Systemic Manifestations of Gluten-Related Disorders

The consequences of this immune dysregulation are not confined to the gut. The war spills over, affecting nearly every system in the body. I strive to make this clear to my patients, especially those who come to me with a constellation of seemingly unrelated symptoms that have baffled other practitioners.

Dermatitis Herpetiformis: Celiac Disease of the Skin

Let’s look closer at dermatitis herpetiformis. We’ve established that the body is churning out IgA antibodies to attack gluten in the gut. But because of the leaky gut, these IgA-gluten complexes don’t stay in the intestine; they circulate in the bloodstream. Due to their size and structure, these immune complexes can become lodged in the tiny blood vessels of the skin, specifically in the dermal papillae.

Once trapped, the immune system detects them as a foreign threat and launches an all-out assault in that localized area. This results in a cascade of inflammatory events:

• Massive inflammation floods the area.
• Mast cells, the “grenades” of the immune system, are triggered to degranulate, releasing histamine and other inflammatory mediators.
• This leads to the characteristic symptoms of DH: intense, maddening itching and burning, followed by the eruption of symmetrical clusters of blisters and papules, most commonly on the elbows, knees, buttocks, and back.

When a patient presents with these skin lesions, it is a powerful clinical clue. DH is essentially pathognomonic for celiac disease. The root cause is not a skin problem; it is an autoimmune reaction to gluten consumption manifesting in the skin. Treating it with topical steroids alone is merely silencing the alarm without putting out the fire. The only true treatment is a strict, lifelong gluten-free diet.

The Systemic Overload: A Body at War with Itself

Whether it’s celiac disease or severe NCGS, the systemic immune activation creates a state of chronic, body-wide turmoil. The immune system is everywhere, all the time. This leads to a state I call “cytokine overload.”

Cytokines are signaling molecules the immune system uses to communicate. In an acute infection, a surge of cytokines is necessary to coordinate a defense. But in a chronic condition like untreated celiac disease, the cytokine production never shuts off. This low-grade but relentless storm of inflammatory cytokines, such as TNF-alpha, IL-6, and IL-1, is what drives the systemic symptoms that make patients feel so profoundly unwell.

This state of constant alarm and inflammation puts an enormous strain on several key systems:

• Adrenal Exhaustion: Your adrenal glands are responsible for producing cortisol, your primary anti-inflammatory and stress hormone. When faced with constant inflammation, the adrenals are forced to work overtime, pumping out cortisol to try and quell the fire. Over time, this can dysregulate the hypothalamic-pituitary-adrenal (HPA) axis, often called adrenal fatigue or exhaustion. This manifests as debilitating fatigue, poor stress resilience, sleep disturbances, and an inability to feel rested.
• Liver Stress: The liver is your body’s primary detoxification organ. It must process inflammatory debris from the immune battle, toxins leaking from the gut, and metabolic byproducts of cellular stress. A chronically overburdened liver can lead to elevated liver enzymes, poor detoxification capacity, and further contribution to systemic toxicity.
• Nutrient Malabsorption: This is the most direct and devastating consequence of villous atrophy in celiac disease. As the intestinal villi flatten and are destroyed by the autoimmune attack, the surface area available for nutrient absorption plummets. Even on a nutrient-dense diet, a person can become severely deficient in critical vitamins and minerals. Common deficiencies include:

• • Iron: Leading to iron-deficiency anemia, causing fatigue, shortness of breath, and pale skin.
  • Calcium, Vitamin D, and Magnesium: Leading to bone loss, osteopenia, and eventually, osteoporosis.
  • B Vitamins (especially B12 and Folate): Crucial for neurological function, energy production, and detoxification. Deficiencies can cause peripheral neuropathy, cognitive issues (“brain fog”), and anemia.
  • Fat-Soluble Vitamins (A, E, K): Essential for immune function, skin health, blood clotting, and antioxidant protection.

I want to be unequivocally clear on this point. There is no magic tea, no special supplement, and no miracle pill that will allow a person with celiac disease to continue eating gluten without consequence. The only “cure” is completely and permanently removing gluten from the diet. The idea of “controlling” it while still consuming the trigger is a physiological impossibility. It’s like trying to patch a bullet wound while someone is still shooting you. You must first stop the assault.

The Threshold Effect: “Why Did This Happen to Me Now?”

One of the most common questions I hear from patients diagnosed with gluten-related disorders in their 30s, 40s, or 50s is, “But Doctor, I’ve been eating bread my whole life. Why is it a problem now?” This is a brilliant question, and the answer lies in a concept known as threshold dynamics.

I often use the bucket analogy to explain this to my patients, and it resonates deeply.

Imagine your gut health as a large bucket. From the day you are born, various factors begin to fill this bucket. Each one adds a small amount of stress to your gastrointestinal and immune systems. These factors include:

• Medications: Antibiotics are a major contributor, as they can decimate beneficial gut flora. Non-steroidal anti-inflammatory drugs (NSAIDs) can directly damage the gut lining. Acid-blocking medications change stomach pH, affecting digestion and microbial balance.
• Dietary Irritants: Beyond gluten, these include excessive sugar, processed foods, industrial seed oils, and other inflammatory ingredients common in the standard modern diet.
• Chronic Stress: Psychological and emotional stress directly and powerfully affects gut health through the gut-brain axis. It can alter gut motility, increase gut permeability, and change microbiome composition.
• Infections: Episodes of food poisoning or other gastrointestinal infections can permanently alter the gut ecosystem.
• Environmental Toxins: Pesticides, heavy metals, and other chemicals in our food, water, and air add to the total body burden.

For decades, your body’s remarkable resilience allows it to manage these insults. Your microbiome, the community of trillions of bacteria in your gut, works hard to maintain balance. Your immune system tolerates minor irritants. The bucket is slowly, imperceptibly filling up, but it hasn’t overflowed. The gut barrier’s integrity, though weakened, is still holding.

Then, one day, the bucket hits its capacity. It could be a particularly stressful period at work, a course of antibiotics, a bout of gastroenteritis, or simply the cumulative burden of decades of small insults. The system’s ability to compensate is finally exhausted. The microbiome becomes significantly dysbiotic (imbalanced), and the tight junctions, which were already strained, finally give way.

Now, the gut has become leaky enough for larger molecules, like the gliadin protein, to spill through the compromised barrier and into the bloodstream in significant quantities. This is the moment the bucket overflows. This is the threshold being crossed.

At this point, the immune system, which may have ignored small amounts of gliadin for years, faces a massive, systemic invasion. It mounts a full-scale response. For those with a genetic predisposition to celiac disease, this is when the adaptive immune system gets the order to create antibodies against TTG. The T-cells, the “special forces” of the immune system, essentially get a PhD in recognizing and attacking your own biology whenever they see gluten-related peptides. The switch has been flipped.

This is why the disease can appear to manifest “out of nowhere” in middle age. Gluten wasn’t ever “fine” for that person; their body’s capacity to tolerate the insult hadn’t been exceeded yet. Understanding the threshold effect is empowering because it shifts the focus from blaming a single trigger to appreciating the cumulative nature of health and disease. It also provides a blueprint for healing: we must not only remove the primary trigger (gluten) but also empty the bucket by addressing other contributing factors.

Eating Right to Feel Better-Video

The Path to Healing: An Integrative and Personalized Strategy

Understanding the “why” and the “how” is the first step. The next, and most crucial, is the “what now?” The good news is that for most individuals, these conditions are manageable and, in the case of NCGS, often reversible.

Step 1: Remove the Offending Agents

• Strict Gluten Elimination (for Celiac Disease): If the diagnosis is celiac disease, the path is non-negotiable: a 100% strict, lifelong gluten-free diet. This means no wheat, rye, barley, or their derivatives. It also requires extreme diligence regarding cross-contamination in kitchens and restaurants. This is the only way to halt the autoimmune attack and allow the body to begin healing.
• Dairy Elimination (The Cross-Reactivity Problem): I strongly advise my patients, especially in the initial phases of healing, to eliminate dairy as well. This is due to a phenomenon called molecular mimicry and cross-reactivity. The protein in cow’s milk, casein, has a molecular structure that can look strikingly similar to gliadin to the immune system. In a hyper-reactive immune state, the body may mistake casein for gluten and launch a similar inflammatory attack (Vojdani & Tarash, 2013). Continuing to consume dairy can be like throwing kindling on a fire you are trying to put out. It prevents the immune system from fully calming down and the gut from fully healing.

Step 2: Healing the Gut Barrier and Rebalancing the System

This is where our integrative approach at Injury Medical Clinic truly shines. Removing the trigger is just the first step. We must then actively work to repair the damage and restore balance to the system. We call this the “4R Program” in functional medicine: Remove, Replace, Reinoculate, Repair.

1. Remove: We’ve already discussed removing gluten and dairy. We also identify and remove other inflammatory triggers, such as pathogenic bacteria, yeast overgrowth (Candida), or parasites, through advanced stool testing.
2. Replace: We support digestive function by replacing what might be missing. This can include digestive enzymes to help break down food properly, or hydrochloric acid (betaine HCl) for those with low stomach acid, which is a common issue.
3. Reinoculate: We work to restore a healthy, diverse microbiome by introducing beneficial bacteria through high-quality, multi-strain probiotics and, more importantly, by feeding those good bacteria with prebiotic fibers from a wide variety of plant foods.
4. Repair: This critical step provides the nutrients needed to rebuild the damaged gut lining. Key nutrients for gut repair include:

• • L-Glutamine: An amino acid that serves as the primary fuel source for the cells of the small intestine.
  • Zinc: Essential for cell regeneration and tight junction integrity.
  • Vitamins A and D: Crucial for immune regulation at the gut barrier.
  • Quercetin, Marshmallow Root, and Slippery Elm: Botanical compounds that have soothing, anti-inflammatory effects on the gut lining.

Step 3: The Role of Chiropractic Care in Systemic Healing

You might be wondering how chiropractic care fits into healing a condition like celiac disease. The connection is through the nervous system. The gut has its own intricate nervous system, the enteric nervous system (ENS), often called the “second brain.” The ENS is in constant communication with the central nervous system (CNS) via the vagus nerve. This communication highway is known as the gut-brain axis.

Structural misalignments in the spine, particularly in the thoracic region where nerves that supply the digestive organs exit, can interfere with this nerve signaling. This interference can disrupt proper gut motility, digestive enzyme secretion, and even the gut’s immune response.

As a Doctor of Chiropractic, my goal is to identify and correct these misalignments, which we call vertebral subluxations, through gentle, specific adjustments. By restoring proper alignment and motion to the spine, we can:

• Optimize Nerve Flow: Reduce interference along the gut-brain axis, allowing for better communication between the central nervous system and the digestive organs.
• Modulate the Autonomic Nervous System: Help shift the body out of a chronic “fight-or-flight” (sympathetic) state and into a “rest-and-digest” (parasympathetic) state. This is crucial for healing, as digestion and repair processes are optimized when the parasympathetic system is dominant.
• Reduce Systemic Stress: A well-aligned body functions more efficiently and adapts better to stressors, which helps “empty the bucket” we discussed earlier.

Chiropractic care is not a direct treatment for celiac disease, but it is a powerful adjunctive therapy that supports the body’s innate ability to heal. It ensures the master control system—the nervous system—is functioning without interference, creating the optimal internal environment for the gut to repair and the immune system to rebalance.

Conclusion: A Reversible Journey for Most

The landscape of gluten-related disorders can seem complex and overwhelming, but I hope this detailed journey has brought clarity and hope. The key takeaway is this: understanding the fundamental difference between the adaptive autoimmune attack of celiac disease and the innate immune irritation of NCGS is the first step toward proper management.

If it is celiac disease, the path is clear: a strict, lifelong gluten-free diet is the medicine. Combined with addressing cross-reactivity and actively healing the gut, this can lead to full symptom remission and halt the autoimmune process.

However, in my clinical experience, most of the time, it’s not even celiac disease. It’s NCGS, driven by a leaky gut and an overburdened system. And the truly wonderful news is that this condition, while debilitating, is often reversible. By removing triggers, healing the gut lining, rebalancing the microbiome, and supporting overall function through an integrative approach that includes functional medicine protocols and chiropractic care, we can guide patients back to vibrant health. We can empty the bucket and teach the body to be tolerant and resilient once more. The journey requires commitment, but the destination—a life free from chronic symptoms—is absolutely within reach.

References

• Fasano, A. (2011). Zonulin and its regulation of intestinal barrier function: The biological door to inflammation, autoimmunity, and cancer. Physiological Reviews, 91(1), 151–175. https://doi.org/10.1152/physrev.00003.2008
• Vojdani, A., & Tarash, I. (2013). Cross-reaction between gliadin and different food and tissue antigens. Food and Nutrition Sciences, 4(1), 20–32. https://doi.org/10.4236/fns.2013.41005
• Zevallos, V. F., Raker, V., Tenzer, S., Jimenez-Calvente, C., Ashfaq-Khan, M., Rüssel, N., Pickert, G., Schild, H., Steinbrink, K., & Schuppan, D. (2017). Nutritional wheat amylase-trypsin inhibitors promote intestinal inflammation via activation of myeloid cells. Gastroenterology, 152(5), 1100-1113.e12. https://doi.org/10.1053/j.gastro.2016.12.006

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