T helper 17 (Th17) cells play a key role in the immune system, particularly in protecting the body from pathogens. They do this by producing interleukin 17 (IL-17), and these cells are critical in maintaining the mucosal barrier and clearing pathogens. However, studies have shown that HIV infection worsens when the Th17 cell population decreases, which has attracted widespread attention in the scientific community.
Loss of Th17 cells leads to a breakdown of the intestinal barrier, which increases the levels of bacterial movement through microbial translocation, exacerbating chronic HIV infection.
Th17 cells play multiple functions in adaptive immunity. They are not only involved in the defense against pathogens, but also play a role in specific pathological processes. The main effector cytokines of these cells include IL-17A, IL-17F, IL-21 and IL-22, which can promote the activation of endogenous immune cells and epithelial cells and participate in the generation and recruitment of neutrophils.
In the context of HIV infection, the loss of intestinal Th17 cells has a significant impact on the overall immune system. These cells not only maintain the integrity of the intestinal epithelium but also effectively prevent bacterial microbial translocation. When the number of Th17 cells decreases, the function of the intestinal barrier is impaired, causing bacteria and endotoxins to escape from the intestine, further triggering systemic immune activation.
Microbial translocation is a major factor causing the aggravation of HIV disease and chronic inflammation.
Microbial translocation is a pathological phenomenon in which microorganisms in the intestine escape through the intestinal barrier into the blood. This process not only results in continued immune system activation, but can also contribute to the worsening of HIV infection. The absence of Th17 cells makes this process more frequent and puts infected individuals at higher risk of pathology.
Recent studies have shown that increasing the number of intestinal Th17 cells may be an effective treatment strategy. It can not only reduce the chronic inflammation caused by microbial translocation, but also support the effectiveness of antiviral treatment. For example, by administering the cytokine IL-21, which promotes Th17 differentiation, researchers have found that they can reduce the extent of microbial translocation and improve the response to highly active antiretroviral therapy (HAART).
Research on regulating Th17 cells provides new perspectives and hope for the treatment of HIV infection.
Although research on Th17 cells shows positive prospects, it also faces many challenges. Specific cellular properties make them more susceptible to HIV infection in the context of infection, leading to loss of function. In addition, excessive Th17 activity may also lead to the risk of autoimmune diseases. Therefore, how to balance the function and quantity of Th17 cells while treating HIV is an important topic for future research.
ConclusionIn summary, Th17 cells play an important role in the pathological mechanism of HIV infection, and their loss triggers multiple chain reactions, aggravating the progression of infection. Faced with this challenge, how can we find effective strategies to restore these important immune cells and thereby improve the health of people infected with HIV?