Background: Malaria, caused by Plasmodium parasites, remains a leading global health concern, impacting millions of people globally. Splenic macrophages are specialized immune cells that reside in the spleen and play a pivotal role in the pathogenesis and immune response during malaria. These cells are fundamental to the body's defense against Plasmodium due to their multifaceted roles in parasite clearance, antigen presentation, and immune regulation. They participate in the early immune response by phagocytosing infected red blood cells, producing cytokines, and interacting with other immune cells to modulate both pro‐inflammatory and anti‐inflammatory responses. Aim: This review highlights the evolving understanding of splenic macrophages in malaria pathogenesis and immunity and underscores their importance in the development of novel therapeutic interventions. Method: The search strategy included retrieving relevant studies from PubMed Central and Google Scholar spanning between 1955–2025. Articles were screened based on relevance to malaria immunology, macrophage biology, and therapeutic interventions. Both experimental and clinical studies were considered, and references from selected articles were also cross‐checked to identify additional relevant literature. Priority was given to peer‐reviewed articles, systematic reviews, and original research that provided insights into the immunological role of splenic macrophages in malaria. Result: Splenic macrophages play a dual role in disease progression and severity. They have a specialized ability to polarize into different functional states under different microenvironments. Notably, macrophage polarization during Plasmodium infection is not strictly dichotomous but exists along a continuum, with macrophages exhibiting both M1 and M2 characteristics, facilitating dynamic immune modulation. This continuum of polarization is essential for balancing immune responses and ensuring effective immunity while avoiding excessive inflammation. Emerging evidence suggests that splenic macrophages significantly influence malaria severity and clinical outcomes, positioning them as key targets for therapeutic strategies. Conclusion: Optimizing macrophage‐mediated immunity by targeting specific macrophage functions and biomarkers could hold promise for improving vaccine development, diagnostics, prognosis, and treatment strategies, thereby enhancing clinical outcomes for malaria patients.

Various immune cells are known to participate in combating infection. Regulatory B cells represent a subset of B cells that take part in immunomodulation and control inflammation. The immunoregulatory function of regulatory B cells has been shown in various murine models of several disorders. In this study, a comparable IL-10 competent B-10 cell subset (regulatory B cells) was characterized during lethal and non-lethal infection with malaria parasites using the mouse model. We observed that infection of Balb/c mice with P. yoelii I 7XL was lethal, and a rapid increase in dynamics of IL-10 producing B220⁺CD5⁺CD1d⁺ regulatory B cells over the course of infection was observed. However, animals infected with a less virulent strain of the parasite P. yoelii I7XNL attained complete resistance. It was observed that there is an increase in the population of regulatory B cells with an increase of parasitemia; however, a sudden drop in the frequency of these cells was observed with parasite clearance. Adoptive transfer of regulatory B cells to naïve mice followed by infection results in slow parasite growth and enhancement of survival in P. yoelii 17XL (lethal) infected animals. Adoptively transferred regulatory B cells also resulted in decreased production of pro-inflammatory cytokine (IFN-γ) and enhanced production of anti-inflammatory cytokine (IL-10). It infers that these regulatory B cells may contribute in immune protection by preventing the inflammation associated with disease and inhibiting the parasite growth.

Malaria remains a major public health problem worldwide. The immune mechanisms that mediate protection against malaria are still unclear. Previously, we reported that mesenchymal stem cells (MSCs) play a critical role in host protection against malaria by altering the dynamic balance of T regulatory cells and effector T cells producing inflammatory cytokines. Here, we report that MSCs reprogram haematopoiesis in primary (bone marrow) and secondary (spleen) lymphoid organs to provide host protection against malaria. Adoptive transfer of MSCs from malaria-infected mice to naïve recipient mice that were subsequently infected with malaria parasites dramatically accelerated the formation of colony-forming units-erythroid cells in the bone marrow. Adoptively transferred MSCs also induced expression of the key erythroid cell differentiation factor GATA-1 in the spleen of recipient animals. Interestingly, we further observed a subtle increase in the CD34⁺ hematopoietic stem and progenitor cells in lymphoid organs, including spleen and lymph nodes. Infusion of MSCs also enhanced T cell proliferation, resulting in increased numbers of both CD4⁺ and CD8⁺ T cells in the spleen. MSCs also inhibited the induction of the negative co-stimulatory receptor programmed death-1 by T cells in recipient animals upon infection with malaria parasites. Taken together, our findings suggest that MSCs play a critical role in host protection against malaria infection by modulating erythropoiesis and lymphopoiesis.

Nitrogen (N) is crucial for plant growth and development; however, excessive use of N fertilizers cause many problems including environmental damage, degradation of soil fertility, and high cost to the farmers. Therefore, immediate implementation is required to develop N efficient crop varieties. Rice being low nitrogen use efficiency (NUE) and a high demand staple food across the world has become a favorite crop to study the NUE trait. In the current study, we used the publicly available transcriptome data generated from the root and shoot tissues of two rice genotypes IR-64 and Nagina-22 (N-22) under optimum N supply (N⁺) and chronic N-starvation (N⁻). A stringent pipeline was applied to detect differentially expressed genes (DEGs), alternatively spliced (DAS) genes, differentially expressed transcripts (DETs) and differential transcript usage (DTU) transcripts in both the varieties and tissues under N⁺ and N⁻ conditions. The DAS genes and DTU transcripts identified in the study were found to be involved in several metabolic and biosynthesis processes. We suggest alternative splicing (AS) plays an important role in fine-tuning the regulation of metabolic pathways related genes in genotype, tissue, and condition-dependent manner. The current study will help in understanding the transcriptional dynamics of NUE traits in the future.