Editorial: Helminthosis – Immuno-pathology and Anthelmintic Vaccines

Joydeep Paul^1*Muhammad Tofazzal Hossain²Md. Aminul Islam²Anisuzzaman Anisuzzaman^2*

• ¹Adamas University, Kolkata, India
• ²Bangladesh Agricultural University, Mymensingh, Bangladesh

Helminth infections remain a major global challenge, especially in the tropics and the sub-tropics. While they rarely receive the attention accorded to tuberculosis or malaria, their burden is considerable, resulting in growth impairment, infertility, chronic disability, and premature mortality (Anisuzzaman and Tsuji., 2020, Frahm et al., 2019, Anisuzzaman et al., 2021). Coevolution of these helminths along with their respective hosts is the key to their survival and persistence, even in the modern world (Yasmin et al., 2025). Initially, helminth infections induce a Th1 immune response, accompanied by increased IgE and T cell activation. Later in the chronic illness, polarization of the host immune response towards Th2 helps the parasites to survive in a more favourable environment (Gazzinelli-Guimaraes et al., 2024). The immune response to the helminths is inherently paradoxical. Protective in some contexts, yet can be manipulated by the parasites to ensure survival (Figure 1). This duality is central to the immunopathology examined in this issue. Helminths also actively induce Treg cells, which helps the helminth's survival by suppressing the host's immune response. Helminth-induced Treg ameliorates "bystander" immune responses, protecting against allergies and autoimmune diseases (Ohnmacht et al., 2015). The pursuit of vaccines is equally important, which, despite decades of work, lags behind efforts against bacterial and viral diseases (Diego et al., 2025). This study offered fresh perspectives on these intertwined challenges. This issue will also help us to understand the host-parasite interactions more intricately by highlighting the underlying molecular mechanisms, particularly in the field of vaccine development. In summary, all ten articles not only provided insights into how helminths use different strategies for their survival in the host, but also suggested diverse approaches that could be used to combat infection. From cellular pathways and EV microRNAs to vaccine antigens and exercise-based interventions, the breadth of inquiry represented here is striking. Importantly, modern understanding unmasked that helminths are not only pathogens but also sources of therapeutic insights, resulting a twist whether helminths are 'friends or foe'. This issue also highlights the ongoing need for increased visibility in helminth research. Despite their enormous global burden, particularly in low and middle-income countries, these diseases risk neglect amid shifting public health priorities. By bringing together diverse work, this collection highlights both the scientific vibrancy of helminthology and its translational relevance for wider immunological and inflammatory conditions.In conclusion, this special issue is more than a compilation of papers. The studies here remind us that advancing vaccines and therapies against these parasites requires scientific rigor but also collaborative persistence. May it inspire further inquiry and innovation in tackling helminthiosis and its far-reaching consequences. Ohnmacht, C., Park, J. H., Cording, S., Wing, J. B., Atarashi, K., Obata, Y., Gaboriau-Routhiau, V., Marques, R., Dulauroy, S., Fedoseeva, M., Busslinger, M., Cerf-Bensussan, N., Boneca, I. G., Voehringer, D., Hase, K., Honda, K., Sakaguchi, S., Eberl, G. (2015). The microbiota regulates type 2 immunity through RORγt⁺ T cells. Science. 349(6251):989-993.Yasmin, H., Datta, P., Deb, A., Willingham, A. L., Kishore, U. (2025). Innate immune response to helminth infections. Adv. Exp. Med. Biol.1476:251-273. Helminthiosis: Immunological orchestra and patho-biology. AAM, alternatively activated macrophage; APC, antigen presenting cell; DC, dendritic cell; SMCs, smooth muscle cells, GCs, goblet cells; Ecs, epithelial cells; FBs, fibroblasts; Incrd, increased; Ag, antigens; BAMs, bioactive molecules, PrX, 2-Cys peroxiredoxin; RELM-α, Resistin-like Molecule-α; PDGF, plateletderived growth factor; IGF-1, insulin-like growth factor 1; HMGB1, High-Mobility Group Box 1, RAGE, receptor for advanced gycation end-products; ESP, excretory-secretory products.