Molecular Pathogens, 2025, Vol.16, No.1, 1-9 http://microbescipublisher.com/index.php/mp 6 disturbed. To solve this problem, we need to understand more about their immune responses in the body when they are infected, such as how cytokines change. This information can help us design more effective vaccines and treatments (Meng et al., 2023). 7 Case Studies of Immune Response to Specific Pathogens 7.1 Brucellosis: immune mechanisms and control measures Brucellosis is a relatively big problem for water buffalo. This disease not only affects the health of water buffalo, but also reduces milk production and fertility. The immune response of buffalo to Brucella is divided into two parts: innate immunity and adaptive immunity. Innate immunity is the body's first line of defense. Some “immune sensors” like NOD-like receptors will discover bacterial components and then initiate an immune response. These receptors trigger a process that allows the body to produce some pro-inflammatory cytokines, which help fight bacterial infections (Brahma et al., 2015). In order to prevent buffalo from being infected with Brucella, the main method is to vaccinate them, and to do a good job in epidemic prevention, such as isolating sick cattle, cleaning the environment, etc., to reduce the chance of virus transmission. 7.2 Foot-and-mouth disease: vaccine development and host immunity Foot-and-mouth disease is a highly contagious disease and is also a major threat to the buffalo group. Therefore, it is very important to develop effective vaccines. To make the vaccine work better, researchers hope it can inspire a strong immune response, including allowing the body to produce antibodies (humoral immunity) and active immune cells (cellular immunity). When first infected, the buffalo's immune system will first use receptors such as NOD1 and NOD2 to recognize the virus. These receptors can activate immune signaling pathways and produce inflammatory responses. In the laboratory, scientists used buffalo immune cells, such as monocytes (PBMCs), macrophages and breast cells in the blood. It was found that after stimulating these cells with NOD receptor agonists, a large number of IFN-γ and proinflammatory factors were produced, indicating that the immune response was successfully initiated (Figure 2) (Brahma et al., 2015). Understanding these mechanisms will help us design stronger and longer-acting vaccines. Figure 2 Comparison of LRR domains of buNOD1 (left panel) and buNOD2 (right panel) (Adopted from Brahma et al., 2015)
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