Smut fungi, such as Ustilago maydis, have been studied extensively as a model for plant-pathogenic basidiomycetes. However, little attention has been paid to smut diseases of agronomic importance that are caused by species of the genus Thecaphora, probably due to their more localized distribution. Peanut smut incited by Thecaphora frezii has been reported only in South America, and Argentina is the only country where this disease has been noted in commercial peanut production. In this work, important advances in deciphering T. frezii specific biology/pathobiology in relation to potato (T. solani), wheat (U. tritici), and barley (U. nuda) smuts are presented. We summarize the state of knowledge of fungal effectors, functionally characterized to date in U. maydis and most recently in T. thlaspeos, as well as the potential to be present in other Thecaphora species involved in dicot-host interactions like T. frezii-peanut. We also discuss applicability and limitations of currently available methods for identification of smut fungi in different situations and management strategies to reduce their impact on agri-food quality. We conclude by describing some of the challenges in elucidating T. frezii strategies that allow it to infect the host and tolerate or evade plant immune defense mechanisms, and assessing other aspects related to pest control and their implications for human health.

Aflatoxin B₁ (AFB₁) and fumonisin B₁ (FB₁) are cereal-contaminating mycotoxins; co-exposure to these compounds is associated with hepatocellular carcinoma, although the underlying immunological mechanisms remain unclear. This study aimed to investigate the impact of AFB₁ and FB₁, individually and combined, on immune cell function, focusing on Th1-associated cytokines, cytotoxic capacity, oxidative stress involvement, and energy and purinergic metabolism. Rat splenocytes and intrahepatic leukocytes were exposed to AFB₁ (20 μM), FB₁ (10 μM), or a mixture of both (MIX), in the presence or absence of catalase. Cytokines and phenotypes were assessed by flow cytometry and ELISA, cytotoxicity by co-culture assays, and intra/extracellular adenine nucleotides and purines by HPLC. The MIX significantly impaired Th1-like differentiation and reduced IFNγ and TNFα production, FAS-L expression and cytolytic activity while increasing IL4 production, indicating a shift toward a Th2-like profile. These effects were prevented by catalase, supporting a key role for oxidative stress. Co-exposure disrupted intracellular energy balance, decreasing adenosine triphosphate (ATP) levels, ATP/ADP ratios, and total adenine nucleotide pools. It also enhanced purine degradation, extracellular ATP release and adenosine accumulation, suggesting altered purinergic signaling. Consequently, AFB₁-FB₁ co-exposure disrupts immune function through interconnected redox and metabolic mechanisms, promoting an immunosuppressive environment that may favor tumor progression.