Scientists have discovered a mechanism for protecting the intestine from cancer using antibodies

The immune system protects the body from infections, but its functions are not limited to fighting pathogens. Some antibodies help maintain a balance between intestinal bacteria and the cells lining the digestive tract. The researchers found that one of these mechanisms can restrain excessive cell proliferation and prevent the formation of colon tumors. The role of antibodies in this and why their absence increases susceptibility to cancer is described in the Izvestia article.

The lack of antibodies increased the number of tumors

The study was conducted by scientists from Rockefeller University in the USA. The results are published in the journal Nature. The team studied immunoglobulin A (IgA), one of the main classes of antibodies produced in the body and present on mucous membranes, including the intestine.

The experiments used mice with IgA deficiency and compared them with animals in which antibodies were produced normally. Both groups were kept in the same conditions and received the same food. Mice without IgA developed more than twice as many colon tumors. The researchers obtained a similar result in several experimental models of colorectal cancer development.

The scientists also found that with oral administration of IgA, the increased susceptibility of mice to tumor formation disappeared. This suggested that antibodies in the intestine not only perform a protective function against bacteria, but also directly participate in the regulation of the cells of its wall.

Antibodies inhibit intestinal cell division

To understand the mechanism, the researchers studied epithelial cells — they line the inner surface of the intestine and are involved in the renewal of its tissues. It turned out that in the absence of IgA, the activity of genes associated with reproduction changed in these cells. Moreover, the changes occurred even before the appearance of tumors.

Scientists have discovered a DMBT1 receptor on the surface of epithelial cells, which IgA can bind to. In the presence of intestinal bacteria, this receptor promotes cell proliferation. However, when antibodies attach to it, the signal stimulating division is limited. Thus, IgA acts as a kind of brake that prevents cells from multiplying excessively.

In the absence of antibodies, this mechanism stops working properly. Epithelial cells continue to respond to the presence of bacteria by increased division, and a violation of control over tissue renewal increases the likelihood of tumor formation. Additional experiments have shown that the protective function depends on the structure of the antibody itself, and not on its ability to bind to certain types of bacteria.

The researchers also found that without intestinal microorganisms or with impaired signaling through DMBT1, the described mechanism did not manifest itself in the same way. This indicates a complex interaction between the microbiome, the immune system, and intestinal cells.

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The protective function of antibodies was unexpected

Previously, immunoglobulin A was primarily considered as part of the body's first line of defense. These antibodies bind to various intestinal bacteria, regulate their interaction with the mucous membrane, and help maintain a balanced microflora. However, new work has shown that IgA is able to directly influence the behavior of intestinal epithelial cells.

One of the authors of the study, Gregory Donaldson, noted that IgA deficiency occurs in about one in 500 U.S. residents and has previously been associated with an increased likelihood of colorectal cancer. New animal experiments help explain the possible biological basis of this relationship.

However, the scientists emphasize that the discovered mechanism does not mean that all cases of IgA deficiency lead to the development of tumors. Many factors influence the formation of cancer, and the results of experiments on mice do not allow us to directly transfer the conclusions to humans.

Scientists are studying the role of immunity in cancer prevention

The researchers believe that the discovery helps to better understand how the intestinal immune system is involved in maintaining tissue health. In particular, it may explain why disruptions in the interaction between antibodies, bacteria, and epithelial cells can increase susceptibility to tumor changes.

The DMBT1 mechanism is of particular interest for further research. This receptor is involved in regulating cell proliferation, and its interaction with IgA helps maintain normal intestinal epithelial renewal. Scientists intend to study in more detail how this process changes when tumors occur and what features of the microbiome can affect the protective function of antibodies.

However, for now we are talking about fundamental research, the main experiments of which were conducted on mice and cell models. The work does not prove that changing the level of IgA or the composition of the intestinal microflora prevents cancer in humans. Further research is needed to verify this mechanism and its significance for human health.