Scientists discovered something new about what happens inside the stomachs of people with celiac disease. When someone eats gluten and has celiac disease, their immune system attacks the intestines. Researchers found that a specific immune chemical called IFN-γ directly tells the gut cells to multiply and grow more than normal. This isn’t just the body trying to fix damage—it’s the immune system actively changing how gut cells work. The discovery helps explain why celiac disease damages the intestines the way it does, and could lead to better treatments in the future.

The Quick Take

  • What they studied: Whether the overgrowth of cells in the intestines of people with celiac disease happens because the body is trying to repair damage, or if the immune system is directly causing the overgrowth
  • Who participated: The study involved human intestinal tissue samples from people with untreated celiac disease and laboratory mice that were genetically modified to study immune responses
  • Key finding: A immune chemical called IFN-γ directly signals intestinal crypt cells (deep cells in the gut lining) to multiply and change how they work, independent of any damage to the upper layer of intestinal cells
  • What it means for you: This finding suggests that celiac disease damage happens through a specific immune pathway that could potentially be targeted with new treatments, though more research is needed before new therapies become available

The Research Details

Researchers examined intestinal tissue from people with untreated celiac disease and looked at which genes and proteins were active in the damaged areas. They found that cells deep in the intestinal lining (called crypts) had turned on genes related to immune responses and turned off genes related to fat processing. To test if this was caused by a specific immune chemical called IFN-γ, they gave this chemical to laboratory mice and saw the same changes happen. They also created special mice that couldn’t respond to IFN-γ and found that these mice didn’t show the same changes, proving that IFN-γ was the direct cause.

Understanding exactly what causes intestinal damage in celiac disease is important because it helps scientists develop better treatments. Instead of just managing symptoms, doctors could potentially block the specific immune chemical causing the problem. This research shows the damage isn’t just a side effect of the body trying to heal—it’s an active process that can be targeted.

This research was published in The Journal of Clinical Investigation, a highly respected medical journal. The study used both human tissue samples and animal models, which strengthens the findings. The researchers used genetic tools to prove cause-and-effect, not just correlation. However, the study doesn’t specify exact sample sizes, and animal studies don’t always translate perfectly to humans.

What the Results Show

In people with celiac disease, the deep cells of the intestinal lining (crypts) showed increased activity of genes involved in immune responses, particularly those controlled by IFN-γ. At the same time, these cells showed decreased activity of genes involved in processing fats and other normal cell functions. When researchers gave healthy laboratory mice the IFN-γ chemical, the same pattern appeared—the crypt cells started multiplying more and their gene activity changed in the same way as in celiac disease patients. This proved that IFN-γ alone could cause these changes. Most importantly, when scientists created mice that couldn’t respond to IFN-γ signals, these changes didn’t happen, confirming that IFN-γ was directly responsible.

The research showed that this immune reprogramming of crypt cells happens independently of damage to the upper layer of intestinal cells (villi). This means the immune system isn’t just reacting to damage—it’s actively changing how the deep intestinal cells function. The shift away from fat metabolism in these cells suggests the immune activation fundamentally changes how crypt cells operate.

Previous research knew that celiac disease caused intestinal crypts to grow larger, but scientists weren’t sure if this was the body trying to repair damage or if something else was driving it. This study answers that question by showing it’s an active immune process. This finding builds on existing knowledge about how immune chemicals affect intestinal health and provides a more complete picture of celiac disease mechanisms.

The study doesn’t provide exact numbers of human tissue samples studied. While mouse studies are valuable, mice don’t always respond exactly like humans do. The research focuses on one specific immune chemical (IFN-γ) and doesn’t explore whether other immune chemicals might also play a role. The study examined untreated celiac disease, so it’s unclear if the same mechanism occurs in people following a gluten-free diet.

The Bottom Line

This research is preliminary and doesn’t yet lead to specific recommendations for patients. However, it suggests that future treatments targeting IFN-γ signaling could be beneficial for people with celiac disease. For now, the established treatment—a strict gluten-free diet—remains the standard approach. People with celiac disease should continue working with their doctors and follow current dietary guidelines.

This research is most relevant to people with celiac disease and their doctors, as it could lead to new treatment options. It’s also important for researchers developing new celiac disease therapies. People without celiac disease don’t need to change anything based on this research. Those with suspected celiac disease should still get tested and diagnosed by a healthcare provider.

This is basic research that explains how celiac disease works at the cellular level. It typically takes 5-15 years for basic research to lead to new treatments that reach patients. Don’t expect new therapies immediately, but this discovery is an important step toward better options in the future.

Want to Apply This Research?

  • For people with celiac disease using a health app, track daily gluten exposure incidents and intestinal symptoms (bloating, pain, digestive changes) to correlate with immune response patterns. Rate symptom severity on a 1-10 scale daily.
  • Use the app to maintain a strict gluten-free diet log and set reminders for checking food labels and cross-contamination risks. This research reinforces why strict gluten avoidance matters—it stops the immune chemical cascade that damages the intestines.
  • Track long-term trends in digestive symptoms and energy levels over weeks and months to see how well the gluten-free diet is working. Share this data with your healthcare provider to monitor intestinal healing, which may eventually be measured through follow-up biopsies.

This research explains how celiac disease develops at the cellular level but does not change current treatment recommendations. If you have celiac disease, continue following your doctor’s advice and maintain a strict gluten-free diet. Do not stop any current treatments or make dietary changes based on this research alone. Anyone with symptoms of celiac disease should be tested and diagnosed by a healthcare provider before making any dietary changes. This article is for educational purposes and should not replace professional medical advice.