**2. Inflammatory response in neurocysticercosis**

Cysticerci triggers an immune response in the CNS, leading to inflammation and the recruitment of immune cells. The inflammatory response can vary depending on the location and stage of the cysticerci. Inflammatory cells, such as lymphocytes, macrophages, and eosinophils, infiltrate the cysticerci and the surrounding brain tissue, forming granulomas [10–14].

The relationship between the inflammatory response and neuropathology in NCC is complex and dynamic. The presence of the larval stage of the pork tapeworm, *T. solium*, in the CNS, triggers an immune response, leading to inflammation. This inflammatory response plays a crucial role in the pathogenesis and progression of NCC [1, 14, 15].

#### **2.1 Immune cell infiltration**

The inflammatory response in NCC involves infiltrating various immune cells into the affected CNS tissue. These immune cells include lymphocytes, macrophages, eosinophils, and occasionally neutrophils. They are recruited to the site of infection in response to the presence of the larval cysticerci [11–14].

#### **2.2 Inflammatory mediators**

Inflammatory mediators play a crucial role in NCC -associated inflammation. Cytokines, chemokines, and other inflammatory molecules are released by immune cells and contribute to the inflammatory response. These mediators include tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and interleukin-10 (IL-10), among others. They regulate immune cell activation, migration, and effector functions [11, 13, 14, 16].
