The new mechanism regulates the immune response against parasites

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Researchers at the University of Liège (Belgium) have uncovered a previously unknown mechanism that regulates the immune response against parasites. During a parasitic infection, specific immune cells known as virtual memory T cells (TVM) become activated and express a surface molecule called CD22, which prevents an excessive immune response. This discovery could help better control inflammation and improve immune responses to infections. Almost a quarter of the world's population is infected by helminths, parasitic worms that establish themselves in the intestines over a long period of time. In response to these invaders, the immune system deploys complex defense strategies. A recent study conducted by a…

The new mechanism regulates the immune response against parasites

Researchers at the University of Liège (Belgium) have uncovered a previously unknown mechanism that regulates the immune response against parasites. During a parasitic infection, specific immune cells known as virtual memory T cells (TVM) become activated and express a surface molecule called CD22, which prevents an excessive immune response. This discovery could help better control inflammation and improve immune responses to infections.

Almost a quarter of the world's population is infected by helminths, parasitic worms that establish themselves in the intestines over a long period of time. In response to these invaders, the immune system deploys complex defense strategies. A recent study conducted by a team of researchers at the University of Liège has revealed a previously unexpected mechanism that regulates the activation of certain immune cells: CD8+ virtual memory T cells (TVM).

A surprising role for CD22 in T cell regulation

The researchers found that in helminth infections, a key immune molecule, interleukin-4 (IL-4), strongly stimulates TVM cells and causes their proliferation in the spleen and lymph nodes. TVM cells are immune cells that are able to respond quickly to viral infections. In a previous study published in 2018, the research team showed that IL-4 stimulation of TVM cells improved viral infection control during helminth-virus co-infections. However, this intense stimulation of TVM cells during a parasitic infection does not appear to play a role in controlling the parasite itself, which intrigued the researchers.

“What is surprising is that this activation of TVM cells is accompanied by the expression of a receptor called CD22, which is normally exclusive to B lymphocytes, another type of white blood cell.”Explains Professor Benjamin Dewals from Uliège."This receptor plays a crucial role in regulating immune responses. Its presence in TVM cells acts as a brake, limiting their excessive activation and thereby preventing excessive inflammation."

A delicate balance between defense and regulation

This discovery opens up new perspectives on how the body regulates its immune responses. In addition to their role in fighting certain infections, TVM cells also help regulate inflammation in parasitic infections. In other words, instead of just responding to IL-4 produced during infection, they also work to prevent the immune system from overreacting.

Understanding this mechanism in more detail may pave the way for new strategies to improve immune defenses against infections or, conversely, to mitigate excessive inflammatory responses responsible for certain autoimmune diseases.“Further research is needed to determine whether a similar phenomenon exists in humans and how this discovery might be applied in medicine.”Adds Professor Dewals.

This study, conducted in collaboration with researchers from Université Libre de Bruxelles, McGill University (Canada) and the University of Erlangen (Germany), highlights the importance of fundamental research in unlocking the secrets of the immune system and potentially leading to breakthrough medical fields.


Sources:

Journal reference:

Yang, B.,et al. (2025). IL-4 induces CD22 expression to restrain the effector program of virtual memory T cells. Science Immunology. doi.org/10.1126/sciimmunol.adk4841.