Numerous factors can disrupt the development and function of the turkey immune system. The post-hatching period is critical because poults are exposed to various substances, microorganisms, and vaccines when their immune system is immature. The aim of this experiment was to determine whether the administration of antimicrobials to young turkeys affects their immune responses. The experiment was designed two-factorially, with four treatments – C (untreated control), M, E, and D –and two vaccination schedules – vaccinated (+) and unvaccinated (−). Groups M+ and M− received the coccidiostat monensin in their diet for 56 days. Groups E+ and E− were administered enrofloxacin, and those from groups D+ and D− doxycycline in drinking water for the first 5 days of life. One-day-old turkeys from groups C+, M+, E+, and D+ were vaccinated against turkey rhinotracheitis and Newcastle disease, and 28-day-old turkeys against Ornithobacterium rhinotracheale. On days 7 and 56, the levels and relative gene expression of selected cytokines, and the percentages of T cells (CD4+, CD8a+, and CD4+CD8a+) and B cells (IgM+) were determined in blood samples, as were the levels of these cells in the spleen. The coccidiostat had no effect on the percentage of the analyzed T- and B-cell subpopulations, but it increased the plasma IL-8 and interferon γ levels in 7-day-old birds. Antibiotics decreased the plasma IL-6 and tumor necrosis factor α levels in 7- and 56-day-old turkeys. Doxycycline increased the splenic percentages of CD8+ and CD4+CD8+ T cells in 56-day-old birds. Enrofloxacin decreased the percentage of B cells and IL-6 gene expression in blood and the plasma levels of IL-1β and IL-2 in the 7-day-old birds. The antibiotics administered to turkeys interfered with the vaccine–immune system interaction by modulating the vaccine-induced response and exerting anti-inflammatory effects. Therefore, administration of antibiotics to healthy poults may suppress immunity, reduce vaccine-induced immunity, and increase susceptibility to infection.