By Andrea Hargraves 
Research conducted by the Institute of Biomedical Sciences of the University of São Paulo (ICB-USP) has revealed that excessive accumulation of a certain defensive cell in the lung is responsible for causing lung tissue damage. This mechanism is the reason behind the exacerbation of tuberculosis cases.
The study was published in the journal Cell reportsIt can serve as a basis for improving the effectiveness of disease treatment.
Mechanism of excessive immune response
- CD4+ T lymphocytes are important defense cells, but in excess they can cause damage.
- Tests conducted on mice carrying virulent tuberculosis and influenza revealed the mechanisms behind the exaggerated immune response.
- A receptor called P2RX7 detects the presence of ATP, which acts as an alert for defensive cell damage.
- This danger signal can trigger an excessive immune response, causing lung tissue damage.
- In summary, lymphocyte accumulation is stimulated by P2RX7.
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Controlling the immune response
The research findings help understand the ideal amount of CD4+ T lymphocytes needed to stimulate recovery from diseases such as tuberculosis, in other words, how to manipulate the cells to make treatment more effective.
Igor Santiago Carvalho, author of the study, highlights the importance of understanding the defense mechanisms present in the body:
The more we can understand the key “players” in the balance between an under-, optimal-, and over-active immune response, the greater the opportunity to manipulate this response through drugs and therapies, with the aim of better controlling the disease and its outcomes.
Igor Santiago Carvalho FAPESP Agency
In 2022, a record number of diagnosed TB cases were recorded. The World Health Organization recorded 7.5 million cases in the year alone. Advances in this field may mean a change in this scenario with the development of alternative treatments.
Next steps
According to Santiago Carvalho, research has discovered that CD4+ T cells can be pathogenic. Now, a phase begins that seeks to understand what drives this increased pathogenesis and how this knowledge can be applied to other diseases. The study was supported by FAPESP.