Increased fruit consumption is associated with reduced risk of inflammatory bowel disease. Little is known about how diet affects T cells during development of colitis. Aronia (Aronia mitschurinii ‘Viking’) berries are rich in polyphenols that putatively modulate inflammatory cytokines. Our objective was to identify the effects of aronia berry consumption on T cell populations in the mouse adoptive transfer model of colitis. Colonic inflammation was induced in recombinase activating gene-1 (RAG)^-/- mice by transfer of CD4⁺CD62L⁺ cells (naïve T cells) from syngenic C57BL6J donors. Upon transfer, RAG^-/- consumed a control diet or diets fortified with 4.5% w/w lyophilized ‘Viking’ aronia berry. Mice were sacrificed 5 or 7 weeks after adoptive transfer to characterize T cell populations by flow cytometery immunohistochemistry. Aronia consumption inhibited colitis-induced wasting at weeks 5-7 after adoptive transfer. At week 4 after transfer, adoptive transfer increased pro-inflammatory T cell populations and increased colonic cytokines. Aronia consumption inhibited colonic IFN-γ and IL-6. Furthermore, aronia increased lamina propria Treg (CD3⁺CD4⁺FoxP3⁺) and Th17 (CD3⁺CD4⁺IL17A⁺) populations. The Th17 population had greater proportions of IL-10⁺ and IL-22⁺ producing cells. Total colonic CD4⁺ was reduced in aronia-fed mice as determined by immunohistochemistry.  At 7-8 weeks after transfer, levels of mesenteric lymph node Th17 had normalized between the control and aronia groups, but increased Treg populations persisted in the aronia groups. Aronia berry consumption appears to inhibit the initiation of adoptive transfer colitis by the modulation of T cells. These changes occur early after adoptive transfer of naïve T cells and prior to extensive colitic weight loss. Increasing Treg and anti-inflammatory Th17 may be a potential dietary strategy to inhibit the onset of colitis.