Immune System: What You Need to Know about Celiac Disease

Discover the effects of celiac disease on the immune system in the body and what it means for those affected by it.

Abstract

Welcome to our educational series. I am Dr. Alex Jimenez, and I am honored to share insights from my extensive clinical experience and the forefront of medical research. In this post, we will embark on a comprehensive journey into the complex world of gluten-related disorders. Many individuals experience discomfort and chronic symptoms without a clear diagnosis, often being told their issues are “all in their head.” My goal today is to demystify these conditions, particularly the critical differences between Celiac Disease and Non-Celiac Gluten Sensitivity (NCGS). We will explore the intricate immunological mechanisms at play, including adaptive versus innate immune responses, and the roles of proteins like gliadin and enzymes like tissue transglutaminase (TTG). We will explore intestinal permeability, or “leaky gut,” and explain how it can serve as a gateway to systemic inflammation and autoimmunity. This journey will cover the physiological underpinnings of symptoms ranging from digestive distress to skin conditions, neurological issues, and nutrient deficiencies. I will also explain the importance of accurate diagnostic testing, the concept of threshold dynamics—why symptoms can suddenly appear later in life—and the critical role of molecular mimicry and cross-reactivity, especially with dairy. Finally, I will illuminate how our integrative approach at Injury Medical Clinic, combining chiropractic care, functional medicine, and collaborative medical oversight, provides a powerful framework for managing and, in many cases, reversing these debilitating conditions. This post is designed to empower you with knowledge, moving you from confusion to clarity and from illness to wellness.

A Message from Dr. Alex Jimenez

Hello, and thank you for joining me. I’m Dr. Alex Jimenez, and throughout my career, which has been enriched by credentials spanning Chiropractic (DC), Advanced Practice Nursing (APRN, FNP-BC), and Functional Medicine (CFMP, IFMCP), I have dedicated myself to understanding the root causes of chronic illness. My clinical observations, honed over years of practice and shared through platforms like chiromed.com and my LinkedIn profile, consistently point to the gut as the epicenter of health and disease.
At our practice, Injury Medical Clinic PA in El Paso, Texas, we have cultivated a unique and powerful multidisciplinary environment. I am privileged to work alongside Dr. Maria Guadalupe Cardenas, MD, a distinguished internist with over 40 years of invaluable experience. Dr. Cardenas (NPI #1164426749, Texas MD License #J2933) serves as our Medical Director and Collaborative Physician, providing essential medical oversight that bridges different healing disciplines. This collaborative model is the cornerstone of modern integrative care. It allows us to seamlessly blend the structural and neurological focus of chiropractic care, the deep diagnostic investigation of functional medicine, and the established standards of internal medicine. Our team approach ensures patients—whether they come to us for personal injury, chronic pain, or complex metabolic issues—receive a truly holistic, comprehensive treatment plan tailored to their unique biology.
Today, I want to guide you through a topic that affects millions yet remains widely misunderstood: the body’s adverse reactions to gluten. The information I’m sharing isn’t just theoretical; it comes from the latest evidence-based research by leading immunologists and gastroenterologists, and it is validated by what we see and successfully treat in our clinic every day. Let’s move beyond the confusion and get to the heart of what’s really happening inside your body.

Celiac Disease vs. Non-Celiac Gluten Sensitivity: Unraveling the Confusion

One of the most significant points of confusion in both conventional medicine and public understanding is the distinction between Celiac Disease and Non-Celiac Gluten Sensitivity (NCGS). Clinicians often treat these two conditions as if they were the same. In reality, they are fundamentally different entities, driven by distinct arms of the immune system and resulting in different long-term consequences. Understanding this difference is the first and most critical step toward proper diagnosis and effective management.

Celiac Disease: An Adaptive Immune Assault on Your Own Body

Celiac Disease is not an allergy or a simple intolerance; it is a genetically predisposed autoimmune disorder. This is a crucial point. When a person with celiac disease consumes gluten, their immune system doesn’t just react to the foreign protein—it launches a full-scale attack against the body’s own tissues. The adaptive immune system orchestrates this response: the highly specific, sophisticated branch of your immunity that involves T-cells and B-cells and creates long-lasting “memory.”
Here is a breakdown of this devastating process:

• The Trigger: Gluten, a protein composite found in wheat, barley, and rye, is the environmental trigger.
• The Immune Response: In genetically susceptible individuals, the immune system mistakenly identifies gluten components as a threat. It then generates highly specific antibodies, primarily Immunoglobulin G (IgG) and Immunoglobulin A (IgA), not just against gluten but against an enzyme in our own body called tissue transglutaminase (tTG).
• The Self-Destruction: This autoimmune response systematically destroys the intestinal villi. These tiny, finger-like projections line the small intestine and absorb nutrients from the food you eat. As the villi become blunted and flattened—a condition known as villous atrophy—the absorptive surface area of the intestine is dramatically reduced.
• The Permanent Nature: A hallmark of the adaptive immune system is memory. Once your body learns to attack its own tissues in response to gluten, that programming is permanent. This is why celiac disease is considered a lifelong condition that requires strict, permanent avoidance of gluten.

The downstream consequences of untreated celiac disease are severe and systemic. The progressive destruction of the intestinal villi leads to profound malabsorption, which can manifest as:

• Osteoporosis: Due to the inability to absorb calcium and Vitamin D.
• Anemia: From impaired absorption of iron, folate, and B12.
• Neurological Damage: Including peripheral neuropathy, ataxia (loss of balance), and cognitive impairment, often linked to nutrient deficiencies and systemic inflammation.
• Cardiovascular Damage: Increased risk of heart conditions driven by chronic inflammation.
• Increased Cancer Risk: Notably, an elevated risk of intestinal lymphomas.

The autoimmune process in celiac disease is a classic example of the immune system’s failure to differentiate between “self” and “non-self,” with devastating consequences for the host.

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

In stark contrast to celiac disease, Non-Celiac Gluten Sensitivity (NCGS) is mediated by the innate immune system. The innate system is our body’s first line of defense. It is rapid and non-specific, designed to react to general patterns of danger or irritation rather than mounting a targeted, memory-based attack.
Think of it this way: if celiac disease is a targeted military strike by special forces (the adaptive immune system), NCGS is more like a riot police response to a street protest (the innate immune system). It is chaotic, inflammatory, and causes significant collateral damage and discomfort, but it is not a calculated mission to destroy the body’s own infrastructure.
In NCGS, the body is not producing antibodies against its own tissue. Instead, the immune system reacts directly to certain components within wheat and other gluten-containing grains. Research has identified several potential culprits:

• Amylase-Trypsin Inhibitors (ATIs): These are non-gluten proteins in wheat that are potent activators of the innate immune system, specifically a receptor called Toll-like receptor 4 (TLR4). TLR4 activation triggers a rapid inflammatory cascade. (Junker et al., 2012).
• Fructans: These are a type of FODMAP (Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols), which are short-chain carbohydrates that are poorly absorbed in the small intestine. In sensitive individuals, gut bacteria rapidly ferment them, leading to gas, bloating, pain, and diarrhea. This suggests that for some people with NCGS, the issue may be more of a carbohydrate intolerance than a reaction to the gluten protein itself.

The key takeaway is that in NCGS, while the symptoms can be severe and overlap significantly with celiac disease (bloating, pain, brain fog, fatigue, joint pain), the underlying mechanism is one of irritation and generalized inflammation, not autoimmune self-destruction. The intestinal villi are not being systematically killed. This is a monumental difference because it means that with proper dietary intervention and gut healing, NCGS is often reversible. The immune system hasn’t developed that permanent, destructive memory.

The Gateway to Systemic Chaos: Unpacking Leaky Gut and the Immune Cascade

To truly grasp how gluten can wreak such havoc, whether in celiac disease or NCGS, we must understand intestinal permeability, more commonly known as “leaky gut.” This is not a fringe theory; leading researchers like Alessio Fasano have identified it as a well-established physiological phenomenon and a prerequisite for autoimmunity (Fasano, 2012).

The Intestinal Barrier: Your Body’s Most Important Wall

Imagine the lining of your small intestine. It is not a thick, impenetrable wall. It is an incredibly delicate, single layer of specialized cells (enterocytes) that separates the chaotic outside world (the contents of your gut) from the sterile, highly regulated environment of your bloodstream. This single-cell layer has a surface area equivalent to a tennis court, all folded up inside you.
These cells are held together by sophisticated protein structures called tight junctions. You can think of these tight junctions as the “glue” or the mortar between the bricks of a wall. Their job is to be selectively permeable—allowing the passage of fully digested micronutrients (vitamins, minerals, amino acids) while blocking undigested food particles, toxins, microbes, and other large molecules. A healthy intestinal barrier guards your internal peace.

Gliadin, Zonulin, and the Breaching of the Wall

This is where gluten enters the scene as a unique and potent saboteur. One of gluten’s primary protein components is called gliadin. For reasons we don’t fully understand, gliadin can interact with the intestinal lining in all humans, regardless of whether they have celiac disease.
Here’s the chain of events that unfolds when gliadin arrives at the gut wall:

1. Gliadin Binds to a Receptor: Gliadin binds to a specific receptor on the surface of the intestinal cells called the CXCR3 receptor.
2. Zonulin Release is Triggered: This binding event sends a signal that triggers the release of a protein called zonulin. Dr. Fasano’s team discovered zonulin and identified it as the master regulator of intestinal permeability (Fasano, 2011).
3. Tight Junctions Are Shredded: Zonulin’s primary function is to “unlock” the tight junctions. It acts like a key that opens the gates between intestinal cells, loosening and separating the junctions.
4. The “Puke“ into the Bloodstream: With the gates wide open, the gut becomes “leaky.” Now, a flood of substances that should have remained within the intestine—bacteria and their toxic byproducts (lipopolysaccharides or LPS), partially digested proteins, and other inflammatory triggers—can “puke” directly into the bloodstream.

This breach of the intestinal barrier is the inciting event. It is the moment a localized gut problem becomes a systemic, body-wide crisis. The immune system, which has 70-80% of its forces stationed just below the gut lining, is immediately alerted to this massive influx of foreign invaders.

The Immune System Goes Ballistic: The Celiac Autoimmune Cascade

In a person with celiac disease, the consequences of this breach are catastrophic. The offending protein, gliadin, now circulates freely in the bloodstream. What happens next is a perfect storm of mistaken identity:

1. Gliadin Gets Tagged: Once in the bloodstream, the gliadin molecule gets “tagged” or modified by the enzyme we discussed earlier, tissue transglutaminase (tTG). tTG attaches to gliadin, forming a new hybrid molecule called a tTG-gliadin complex.
2. A Declaration of War: The immune system’s surveillance cells (antigen-presenting cells) see this tTG-gliadin complex as a highly dangerous foreign entity and present it to the adaptive immune system.
3. Antibodies Are Created: The adaptive immune system responds by producing large amounts of IgG and IgA antibodies designed to find and destroy this tTG-gliadin complex.
4. The Tragic Error of Molecular Mimicry: Here is the crucial error. The immune system becomes so fixated on this target that it can no longer differentiate between the invading complex (tTG-gliadin) and the body’s own native tissue transglutaminase enzyme, which is found throughout the body. The antibodies begin attacking both.
5. Friendly Fire on a Massive Scale: Where does our own tTG enzyme exist in high concentrations?
   • The Intestinal Villi: This is why the gut is the primary site of destruction, leading to villous atrophy.
   • The Endothelium: The delicate lining of our blood vessels, which explains the link to cardiovascular damage.
   • The Skin: Specifically, the dermal papillae, which leads to the skin manifestations of celiac disease.
   • The Brain and Nervous System: Explaining the neurological symptoms.

The immune system, in its effort to eliminate the gluten invader, ends up waging a relentless war on the body’s own critical structures.

The Skin Connection: Dermatitis Herpetiformis

The process gets even more complex and agonizing. Remember those IgA antibodies being produced in the gut to grab onto gluten? With a leaky gut, these IgA-gluten complexes escape the gut and enter the systemic circulation. They are like little inflammatory packets traveling through your blood.
These complexes are eventually filtered out by the tiny blood vessels in the skin, where they get trapped in the dermal papillae (the uppermost layer of the dermis). The immune system detects these trapped complexes and goes absolutely ballistic, right there in your skin. This triggers a localized, but incredibly intense, inflammatory reaction:

• Mast Cell Degranulation: Mast cells, which are packed with histamine and other inflammatory chemicals, explode and release their contents.
• Intense Inflammation: This causes the characteristic symptoms of Dermatitis Herpetiformis (DH), the skin manifestation of celiac disease: severe, symmetrical itching and burning, followed by blisters, typically on the elbows, knees, back, and buttocks.

When a patient presents with DH, they don’t just have a skin problem. They have a systemic autoimmune disease driven by gluten, and their skin is screaming for help. They feel awful all over because this immune activation is not confined to the skin. It creates a body-wide cytokine overload. Cytokines are the immune system’s signaling molecules, and when they are released in excess (a “cytokine storm”), they cause systemic symptoms like profound fatigue, brain fog, body aches, and feverishness. This chronic state of alarm leads to adrenal exhaustion, places immense stress on the liver (which has to process all the inflammatory debris), and, of course, perpetuates the cycle of nutrient malabsorption.

Getting the Diagnosis Right: The Critical Importance of Proper Testing

Given the profound differences between celiac disease and NCGS, accurate diagnosis is not just an academic exercise—it is essential for determining the correct treatment path and prognosis. Unfortunately, many patients fall through the cracks because of improper testing protocols.
The gold standard screening test for celiac disease is a blood test that measures antibodies against tissue transglutaminase, specifically the Tissue Transglutaminase IgA (tTG-IgA) test. This test is highly sensitive and specific for celiac disease.
However, there is a giant, flashing red warning sign that comes with this test, one that is tragically often missed: To get an accurate result, the patient must be actively and regularly consuming gluten for at least four weeks leading up to the test.
Let me explain why. The tTG-IgA test doesn’t measure gluten; it measures the body’s autoimmune reaction to gluten. If you have removed gluten from your diet, the trigger for the autoimmune response is gone. The immune system will calm down, and antibody production will plummet. If you then take the test while gluten-free, it will come back negative. This is a false negative, and it is utterly worthless. It can lead a person with true celiac disease to believe they are fine, leading them to reintroduce gluten and unknowingly continue the path of autoimmune destruction.
In my practice, I have seen countless patients who were told they tested negative for celiac, only to discover they had taken the test after already going gluten-free on their own. This is a critical failure in patient education. If celiac disease is suspected, a “gluten challenge” is mandatory for accurate serological testing. If the blood test is positive, it is typically confirmed with an endoscopic biopsy of the small intestine to look for the characteristic villous atrophy.
For NCGS, the diagnostic process is different. No single biomarker or test currently diagnoses NCGS. It is a diagnosis of exclusion. This means we must first definitively rule out celiac disease and wheat allergy. After that, the diagnosis is confirmed by observing a clear improvement in symptoms on a strict gluten-free diet and a recurrence of symptoms upon a gluten re-challenge.

The Threshold Effect: “Why Is This Happening to Me Now?”

A question I hear almost daily from patients in their 30s, 40s, or 50s who are newly diagnosed with a gluten-related disorder is, “But Doctor, I’ve been eating bread my whole life without a problem. Why is this happening to me now?”
The answer lies in a concept I call threshold dynamics. It’s a powerful analogy that helps patients understand the gradual, cumulative nature of chronic disease.
Imagine your gut health as a bucket. From the day you are born, that bucket begins to fill up with various stressors slowly:

• Medications: Antibiotics, NSAIDs (like ibuprofen), and acid blockers are notorious for damaging the gut lining and disrupting the microbiome.
• Dietary Irritants: Processed foods, sugar, industrial seed oils, and for some, proteins like gluten and dairy.
• Chronic Stress: Psychological and emotional stress directly harms gut function via the gut-brain axis, increasing permeability and inflammation.
• Infections: Past gastrointestinal infections can leave a lasting impact on the gut ecosystem.
• Environmental Toxins: Pesticides, heavy metals, and other chemicals we are exposed to daily.

For decades, your body’s remarkable resilience and compensatory mechanisms manage this load. Your microbiome fights to maintain balance, and your immune system cleans up the messes. But all the while, the bucket is slowly, imperceptibly filling up. Your intestinal barrier weakens, and the diversity of your beneficial gut bacteria dwindles.
Then, one day, the bucket reaches its capacity. It might be a particularly stressful period, a course of antibiotics, or simply the cumulative burden of decades of low-grade insults. The bucket overflows. At this point, the intestinal barrier is sufficiently compromised—it is “leaky” enough for larger molecules like gliadin to spill through the tight junctions in significant quantities.
This is the threshold moment. The gliadin that was previously being managed now pours into the bloodstream, igniting the massive immune response we’ve discussed. For the celiac patient, the adaptive immune system is now activated, and the T-cells effectively earn a “PhD” in attacking the body’s own biology whenever they see gluten-related peptides. For the NCGS patient, the innate immune system is overwhelmed, triggering systemic inflammation. The symptoms that had been simmering below the surface for years explode into clinical reality. It wasn’t that the gluten was harmless before; it was that your body’s defenses were able to contain the damage—until they couldn’t anymore.

Eating Right to Feel Better-Video

The Critical Role of Cross-Reactivity and Molecular Mimicry

When I advise my patients with confirmed celiac disease or severe NCGS to stop eating gluten, the very next sentence out of my mouth is, “And you need to cut out dairy, at least for now.” This often elicits looks of dismay, but the recommendation is based on solid immunological science: cross-reactivity and molecular mimicry.
Molecular mimicry, as we’ve touched on, is the phenomenon where a foreign protein (like gliadin) looks so similar in its amino acid structure to one of the body’s own proteins (like tissue transglutaminase) that the immune system gets confused and attacks both.
Cross-reactivity is a related concept. It occurs when the antibodies generated against one protein (e.g., gliadin) mistakenly react with another, different protein because parts of their structures are very similar. The immune system’s antibodies are like keys looking for a specific lock (the antigen). In cross-reactivity, a different protein has a lock that is so similar to the original target that the antibody “key” fits and turns it, triggering an immune reaction.
The most clinically significant cross-reactant to gluten is casein, the primary protein found in milk and dairy products. Casein’s protein structure bears a striking resemblance to that of gliadin. For a significant percentage of people with gluten sensitivity, their anti-gliadin antibodies will also bind to casein. (Vojdani & Tarash, 2013).
What does this mean in practical terms? It means that even on a 100% strict gluten-free diet, if you still consume dairy, your immune system may remain activated. You are essentially pouring gasoline on the inflammatory fire, just from a different can. The body thinks it’s seeing gluten, and the inflammatory cascade continues, preventing the gut from healing and symptoms from resolving. This is one of the most common reasons why patients fail to get better on a gluten-free diet alone.
That is why, in my functional medicine protocols, removing both gluten and dairy is a non-negotiable first step for at least 60-90 days to allow the immune system to calm down and the gut to begin healing. Other common cross-reactants can include corn, oats (even gluten-free oats, due to a protein called avenin), yeast, and sometimes even coffee. Advanced testing can help identify these, but the gluten-dairy connection is by far the most prevalent and important to address.

The Integrative Chiropractic and Functional Medicine Solution: A Pathway to Healing

The beauty of understanding these complex mechanisms is that it provides us with a clear roadmap for healing. The situation I’ve described, while dire, is manageable and, in the case of NCGS, often completely reversible. This is where our integrative model at Injury Medical Clinic truly shines. We don’t just treat symptoms; we address the root cause from multiple angles.
Our approach is built on functional medicine principles, often summarized by the 5R Program: Remove, Replace, Reinoculate, Repair, and Rebalance.

1. Remove: Eliminating the Triggers

This is the essential first step. We must remove the substances driving inflammation and immune dysregulation.

• Gluten and Dairy: As discussed, this is paramount. Strict elimination is required. We provide patients with extensive education on reading labels, avoiding cross-contamination, and navigating a gluten-free lifestyle.
• Other Food Sensitivities: We may use advanced food sensitivity testing (like IgG or lymphocyte reactivity testing) or a comprehensive elimination diet to identify other patient-specific food triggers.
• Pathogens: If we suspect underlying gut infections (like parasites, bacterial overgrowth (SIBO), or yeast overgrowth), we will use advanced stool testing (like GI-MAP) to identify and then use targeted antimicrobial herbs or, when necessary, prescription medications to eradicate them.

2. Replace: Restoring Digestive Function

Chronic gut inflammation impairs the body’s ability to produce digestive enzymes and sufficient stomach acid. You cannot heal the gut if you cannot properly digest your food.

• Digestive Enzymes: We often supplement with broad-spectrum digestive enzymes to help break down fats, proteins, and carbohydrates, taking the burden off the compromised gut.
• Stomach Acid Support: Many people with gut issues have low stomach acid (hypochlorhydria). Supporting acid levels with betaine HCl can be critical for proper protein digestion and sterilizing the stomach against pathogens.

3. Reinoculate: Rebuilding the Microbiome

A healthy gut barrier is dependent on a healthy, diverse microbiome. The “good bugs” help regulate immunity, produce anti-inflammatory compounds, and reinforce the gut lining.

• Probiotics: We use high-quality, multi-strain probiotics to reintroduce beneficial bacteria.
• Prebiotics: Even more importantly, we focus on “feeding” the good bacteria with prebiotic fibers found in foods like asparagus, onions, garlic, and jicama. This encourages the growth of the patient’s own native beneficial flora.

4. Repair: Healing the Gut Lining

This is where we provide the specific nutrients needed to rebuild the damaged intestinal wall and “re-glue” the tight junctions. Key therapeutic nutrients include:

• L-Glutamine: This amino acid is the primary fuel source for intestinal cells and is critical for repairing the gut lining.
• Zinc Carnosine: A specialized form of zinc that is incredibly effective at healing the gut mucosa.
• Deglycyrrhizinated Licorice (DGL), Aloe Vera, and Marshmallow Root: These soothing herbs provide a protective, anti-inflammatory coating for the gut lining.
• Vitamins A and D: These vitamins are crucial for immune regulation at the gut level and for supporting mucosal health.

5. Rebalance: Addressing Lifestyle and Systemic Imbalance

Healing the gut is not just about diet and supplements. We must address the whole person.

• Stress Management: As stress is a major driver of leaky gut, we incorporate techniques like meditation, deep breathing, and mindfulness.
• Sleep Optimization: Sleep is when the body does its primary repair work. We ensure patients are getting adequate, high-quality sleep.
• The Role of Integrative Chiropractic Care: This is a unique and vital component of our approach. The gut and nervous system communicate constantly via the gut-brain axis. Chronic inflammation and pain signals from the gut can bombard the central nervous system, leading to a state of “central sensitization,” where the nervous system is stuck in a high-alert, “fight-or-flight” mode. This not only perpetuates pain and anxiety but also directly impairs gut function by shunting blood away from the digestive organs.
  • Chiropractic adjustments, particularly to the thoracic and lumbar spine where sympathetic nerves to the gut originate, can profoundly affect this process. By restoring proper spinal mechanics and reducing nerve interference, we can help down-regulate the sympathetic nervous system and promote the “rest-and-digest” parasympathetic state. This improves blood flow to the gut, enhances motility, and reduces the pain signals being sent to the brain.
  • As a chiropractor and a family nurse practitioner, I am uniquely positioned to see how structural alignment directly influences physiological function. Correcting spinal subluxations is not just about back pain; it is about restoring the neurological communication that governs every organ in the body, including the gut. This foundational step in rebalancing the system is often overlooked in conventional and even functional medicine settings.

Dr. Cardenas’s collaborative oversight ensures this entire process is medically sound. She reviews complex cases, helps manage any necessary prescription medications, and provides the internist’s perspective, ensuring that our functional and chiropractic interventions are safely and effectively integrated with the highest standard of medical care. This multidisciplinary synergy allows us to create a truly personalized and robust healing protocol that addresses the patient from structure to cell, from mind to microbiome.
The path to healing from gluten-related disorders is a journey, not a sprint. It requires commitment and guidance. But armed with the right knowledge and a comprehensive, integrative approach, recovery is not just possible—it is expected. All of this is manageable, and if your condition is not celiac disease, it is very often reversible. And the most encouraging news of all is that, in my clinical experience, most of the Hope datasets are manageable, and there is a clear path forward.

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
• Fasano, A. (2012). Leaky gut and autoimmune diseases. Clinical Reviews in Allergy & Immunology, 42(1), 71–78. https://doi.org/10.1007/s12016-011-8291-x
• Junker, Y., Zeissig, S., Kim, S. J., Barisani, D., Wieser, H., Leffler, D. A., Zevallos, V., Libermann, T. A., Dillon, S., Freitag, T. L., Kelly, C. P., & Schuppan, D. (2012). Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4. Journal of Experimental Medicine, 209(13), 2395–2408. https://doi.org/10.1084/jem.20102660
• 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

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