Ascaridia galli is the largest gut-dwelling helminth of chickens which confers adverse effects on meat and egg production and thus, on the animal protein supply and the economy. Both adult and immature parasites affect the gut health, but larval stages play the major role in pathology. The larvae cause excessive mucus production, damage to the intestinal gland, hemorrhage, anemia, diarrhea, and malnutrition. The adult worms can cause death by intestinal obstruction and intussusception. Although both cellular and humoral immunity are involved in fighting against ascaridiasis, the role of naturally acquired immunity is poorly defined. In cellular immunity, Th-2 cytokines (IL-4, IL-5, IL-9 and IL-13), goblet cells (mucin), GALTs (gut -associated lymphoid tissues), CD8α+ intraepithelial cells, TCRγδ+T cells, and TGF-β4 form a protective band. Type 2 immunity provides protection by forming a network of eDAMP (endogenous damage-associated molecular pattern), chitin, and parasitic antigens. Among antibodies, IgY is the most prominent in chickens and provides temporary humoral protection. During parasitic infection, infiltration of various immune cells is evident, especially in the intestinal epithelium, lamina propria, and crypts of the duodenum and jejunum. In chickens older than 3 months, gradual reduction of worm burden is more successful. Female chickens exert a short-lived but higher level of protection by passing IgY to chicks in the form of egg yolk antibodies (EAB). In laying condition, immunity differs greatly between breeds. This review provides a good overview of the silent but inevitable pathological changes induced by A. galli; and the interaction of host immunity with the parasite.