Amongst several studies, a collection of work mainly focusses about the modulation and signalling pathways of immune system engages during the pathogen exposure and chronic infection. Hence, study understanding the immune profile of individuals living in endemic area of infectious diseases (DOI: 10.3389/fimmu.2025.1547854) depicts that repeated exposure of the pathogen could alter the immunity and generated "memory/trained" immune sentinels is a double-edged sword for the host. It mimics the conditions which is possibly find in the infectious-setting region, where low-grade infection persists despite of the active immune system.Similarly, another work on sepsis-induced immunosuppression (DOI: 10.3389/fimmu.2025.1577105) detailed about the progression of the infection and paralysing the immune system due to impaired antigen presentation, alteration in T-cell function. The latter led to the secondary infection resulting in the vulnerability. These observations point out that outcome of infection not only rely on the first/initial pathogen encounter and its clearance but also depends upon the role of functions of the immune responses. This highlights the importance of monitoring the immune system even after the phase of infection, as 37 immune responses continue to evolve. 38Several studies investigated the reprogramming of host responses due to pathogen 40 exposure and chronic infections in this collection. First study evaluated the immune profiles of 41 individuals residing in the regions (DOI: 42 10. 3389/fimmu.2025.1547854). This work demonstrated that continuous or repeated pathogen 43 exposure can alter the immune cells of immune system, begetting the partial 44 "trained/memorized" immune status. This could be sword having the double edge that affects 45 both susceptibility and severity of diseases. This finding aligns with broader observations in 46 endemic infectious-disease contexts, where immune phenotypes represent an equilibrium 47 between protection and low-grade chronic inflammation. 48Another study addressed oral lichen planus (DOI: 10.3389/fimmu.2025.1553963), a chronic 49 inflammatory mucosal disease whose pathogenesis is under-explored. By using single-cell 50 RNA sequencing, SFRP2 + fibroblasts identified as the origin of inflammatory fibroblasts in the 51 lesion and specifically expressed Wnt5a on a subset of these cells and associated with antigen 52 processing and presentation pathways. Also, SFRP2 + Wnt5a + fibroblasts were found to amplify 53 and maintain local immune inflammation through close interactions with CD8 + T cells and 54 epithelial cells. Also, this study showed the upregulation of pro-inflammatory and antigen-55 presentation-associated molecules, including CXCL12, CXCL14, HLA-A, HLA-B, HLA-C, 56 and ERAP2, in the oral lichen planus samples. Collectively, these observations suggested not 57 to consider fibroblasts as merely structural cells in this disease. And accounts as an important 58 cell which shapes the inflammatory microenvironment to help sustain the chronic immune 59 activation. 60There have been submissions in this collection demonstrating mechanism(s) of infectious and 62 autoimmune diseases. Article addressing the intersection of influenza infection and 63 autoimmunity (DOI: 10.3389/fimmu.2025.1558386) to investigates the role of viral insults that 64 may initiate or exacerbate autoimmune signalling, through the several approaches of molecular 65 mimicry, bystander activation, or tissue-specific inflammation. This study highlights that 66 occurrence of autoimmune phenomena in many cases may not trigger in isolation but arises 67 due the involvement of multifactorial signalling cascades of immune sentinels and inherent 68 host susceptibility. Furthermore, an article on thymosin-α1 discuss its role in modulating immune-inflammatory 83 responses (DOI: 10.3389/fimmu.2025.1571456) that selective immunomodulation may aid in 84 controlling excessive inflammation during maintaining protective immunity in the critical-care 85 and post-infection scenario. In nutshell, the efficacy of immunomodulation in any 86 infectious/pathogenic condition mainly relies on respective diseases context or the resulted 87 microenvironment wherein vivid immune sentinels have defined role, and not depends upon 88 immunosuppressive or stimulatory approaches. Further, combining immunological readout, 89 alongside multi-omics data and longitudinal studies can help in revealing the pattern of immune 90 response over the time and disease pathogenicity. Simultaneously, currently in experimental 91 phase of machine learning and AI integration may advisable in identifying a disease-specific 92 immune signature for the development of personalized drug therapeutics. 93This research topic compiles a numerous study to help us better understand how does immune 95 system work, especially during the infectious and inflammatory conditions. Thorough 96 observation from clinical, systemic, and mechanistic point-of-view of an infection emphasizes 97 the complexity of immune system and the specialized role of distinct immune cell niches. 98Connecting these dots can help bridge the gap between basic and translational research while 99 aligning them with clinical practice on a uniform platform. Furthermore, insights gained form 100 experimental studies and real-world longitudinal data can strengthen health care system by 101 enabling the development of improved diagnostic tools, target specific therapeutics, and 102 effective prevention strategies. Overall, in today's AI world, a deeper understanding of the