The progression of fungal co-infection with COVID-19 depends on the patient's genetic innate immunity. Our goal is to understand the connection between the single nucleotide polymorphisms (SNPs) rs5743708 and rs16910526 in the toll-like receptor 2 (TLR2) and dectin-1 (CLEC7A) genes, respectively, and fungal infection in COVID-19 patients.

Systemic lupus erythematosus (SLE) is a chronic, multisystem autoimmune disease whose treatment is still a challenge. The latest registration of anifrolumab for the treatment of moderate-to-severe SLE raises hopes because of its novel anti-interferon mechanism of action. Anifrolumab, a human monoclonal antibody, selectively binds the interferon (INF-) receptor, inhibiting systemic inflammation moderated by interferon pathways. The article presents the first case of an 18-year-old man with severe, relapsing and repeatedly hospitalized SLE, successfully treated with anifrolumab. During a subsequent exacerbation with multi-organ involvement, which could not be controlled despite pulses and high doses of glucocorticoids (GCSs), treatment with anifrolumab was initiated. Clinical improvement was achieved 4 weeks after the first dose. The patient's dose of systemic GCSs was gradually reduced until complete withdrawal. No serious side effects were observed throughout the follow-up period, and the criteria for complete remission were achieved by the patient at month 3 of therapy. After 12 months, therapy was discontinued due to a payer decision. Nevertheless, the patient remains in follow-up 14 months after the completion of therapy on stable treatment with hydroxychloroquine and azathioprine. He is still not taking prednisone. This is the first case in Poland to show the fate of a "real life patient" after completion of anifrolumab therapy, an effective clinical remission of many months without the use of oral GCSs.

T cell immuno-metabolic regulation plays a key role in the development of systemic lupus erythematosus (SLE). This study aimed to analyze the role of CD4 T cell glucose metabolism in SLE development.

Cardiotoxicity caused by immune checkpoint inhibitors is one of the most severe and potentially fatal side effects. Hence it is crucial from a therapeutic standpoint to understand the underlying processes and devise countermeasures. This study sought to determine whether the SOCS3/JAK/STAT3 signaling pathway, which controls macrophage polarization, contributes to the cardiotoxicity caused by PD-1/PD-L1 inhibitors. The PD-1/PD-L1 inhibitor BMS-1 (10 mg/kg) was used to create a mouse model of immune checkpoint inhibitor-related cardiotoxicity, and hematoxylin and Masson's trichome tests were used to measure cardiomyocyte apoptosis and cardiotoxicity. The production of M1 factors (tumor necrosis factor [TNF-] and interleukin [IL]-1 ), as well as the blood levels of myocardial enzymes (creatine kinase, aspartate transaminase, creatine kinase-MB, and lactate dehydrogenase), were evaluated by ELISA. Echocardiography was used to assess the heart's health. The processes were investigated using flow cytometric analysis, real-time PCR, Western blot, and chromatin immunoprecipitation. We found that the PD-1/PD-L1 inhibitor BMS-1 dramatically reduced tumor weight while considerably impairing cardiac function in melanoma-induced tumor-bearing mice. At the gene and protein levels, it was found that levels of SOCS3, JAK, STAT3, and the inflammatory mediators IL-6 and TNF- had all significantly decreased. Immune checkpoint inhibitor-induced cardiotoxicity may be linked to major changes in the SOCS3/JAK/STAT3 signaling pathway, as indicated by the knockdown of SOCS3, JAK, and STAT3. Finally, immune checkpoint inhibitor intervention demonstrated a large elevation of CD86+ and MHCII+ as well as a considerable increase in macrophages. These data suggest that the SOCS3/JAK/STAT3 signaling pathway, which controls macrophage polarization, may be linked to cardiotoxicity caused by PD-1/PD-L1 inhibitor therapy.

Macrophages are the primary cells of the mononuclear system. Studies have demonstrated that macrophages play an active role in the pathophysiology of cancers due to their remarkable adaptation capacities. The objective of this investigation was to examine the impact of apelin on macrophage polarization in the colon cancer microenvironment.

Polycomb repressive complex 1 (PRC1) is a crucial epigenetic modification complex that plays significant roles in embryonic development, cell differentiation, and tumorigenesis. However, its predictive value and role in immunotherapy remain unclear.

Inflammatory bowel disease (IBD) is a chronic and recurrent autoimmune condition. Numerous studies have reported that non-coding RNA, especially long non-coding RNA (lncRNA), plays a significant role in the regulation of IBD. This study sought to investigate the expression of lncRNA DDX11-antisense RNA 1 (DDX11-AS1) in IBD and its potential diagnostic value, while also evaluating the influence of DDX11-AS1 on the functionality of colorectal mucosal cells.

Dermatomyositis (DM) is the most prevalent disease among myositis patients. The immune response is crucial in DM development. Bioinformatics research on immune-related genes in DM is limited. This study attempted to construct a diagnostic model and investigate immune characteristics of immune-related differentially expressed genes (DEGs), which could aid in DM diagnosis.

The immunopathogenesis of rheumatoid arthritis (RA) is greatly affected by macrophages. However, the precise mechanisms by which selenium-binding protein 1 (SELENBP1) regulates the interaction between macrophages and synovial fibroblasts remain incompletely understood.

Rheumatoid arthritis (RA) is a chronic autoimmune disease that, if uncontrolled, leads to progressive joint damage. The potential immunomodulatory effects of COVID-19 vaccination on autoimmune disease activity remain an area of investigation.

In the landscape of tumor immunotherapy, T cell-mediated immune responses have consistently captured the attention, while the contributions of B cells have been neglected. Nevertheless, growing evidence underscores the pivotal role of tumor-infiltrating B cells and plasma cells, collectively termed tumor-infiltrating B lymphocytes (TIL-B), in cancer treatment. These cells not only contribute significantly to therapeutic outcomes and prognostication in the realms of standard treatment and immune checkpoint inhibition but also open avenues for novel immunotherapeutic strategies. Interestingly, the heterogeneity within TIL-B populations, marked by diverse phenotypic subgroups, provides them with the capacity to exert both antitumor and protumor influences. Therefore, a comprehensive understanding of TIL-B interactions with tumors would be helpful for harnessing TIL-B as targets in tumor immunotherapy. Here, we survey the current state of TIL-B research with the aim of elucidating their role in tumor immunotherapy and offering insights for the development of TIL-B-based therapeutic approaches.

The PD-1/PD-L1 immune checkpoint pathway plays a critical role in tumor immune escape and disease progression. This study investigated differences in tumor-infiltrating lymphocytes (TILs) and PD-L1 expression between primary breast cancers and matched metastatic lesions, and their relationships with clinical outcomes.

Although generalized edema is a rare adverse event after drugs or vaccinations, here we report a case of generalized edema with systemic inflammatory reaction clinically similar to incomplete systemic capillary leak syndrome (SCLS), potentially triggered by COVID-19 immunization. The patient presented with generalized subcutaneous edema, a drop in blood pressure, elevated inflammatory biomarkers, and hypoalbuminemia after receiving the vaccine, with no other apparent cause than vaccination. Comprehensive diagnostic evaluation revealed no specific underlying cause. She was treated with glucocorticosteroids successfully. This case underscores the importance of recognizing rare but severe adverse events associated with vaccinations. Given the widespread administration of COVID-19 vaccines, it is crucial to identify and understand such reactions to ensure timely diagnosis and management. Therefore, we review the existing cases of SCLS following COVID-19 vaccination. Our review highlights the need for heightened vigilance and further research into the mechanisms underlying vaccine-induced phenomena to improve patient outcomes and vaccine safety profiles.

This study aimed to investigate the mechanisms of innate immunosenescence in elderly patients with sepsis and to evaluate the potential application of innate immune modulation strategies in clinical management. Through a literature review, the characteristics of sepsis in the elderly, the aging mechanisms of the innate immune system, the impact of immunosenescence on susceptibility to sepsis, and clinical management strategies for sepsis in the elderly were analyzed. The incidence and mortality rates of sepsis in the elderly increase significantly with age, closely related to the severity of infection, the high prevalence of comorbidities, atypical symptoms, and a greater risk of multi-organ failure. Innate immunosenescence, including the decline in function of neutrophils, monocytes/macrophages, natural killer cells, and dendritic cells, is a key factor in the increased susceptibility to sepsis in the elderly. Immunomodulatory treatments, such as granulocyte colony-stimulating factor (G-CSF), interferon (IFN-), and granulocyte-macrophage colony-stimulating factor (GM-CSF), show potential in improving the prognosis of elderly patients with sepsis and reducing mortality rates. The management of sepsis in the elderly requires a comprehensive approach that takes into account age-related physiological and pathological changes, as well as early diagnosis and proactive intervention measures. Immunomodulatory strategies targeting the unique characteristics of immunosenescence in the elderly offer new avenues for improving survival rates and treatment outcomes in elderly patients with sepsis.

Growing evidence suggests that long non-coding RNA (lncRNA) GAS5 plays a critical role in inflammatory responses such as arthritis. In this study, we explored the function of GAS5 in acute gouty arthritis (AGA) and elucidated how GAS5 acts.

Severe pneumonia in children is a rapidly progressing respiratory system disease. If not promptly controlled, it can lead to respiratory failure, posing a serious threat to the child's life. This study investigated the diagnostic and prognostic potential of miR-192-5p in children with severe pneumonia and respiratory failure.

Excessive release of inflammatory cytokines in severe infections significantly contributes to the onset and progression of sepsis, a condition linked to elevated mortality rates in intensive care units. However, the lack of effective sepsis treatment strategies remains a significant challenge in critical care medicine. The use of anti-inflammatory agents against sepsis has advantages. Urinary trypsin inhibitor (UTI), a serine protease inhibitor obtained from the urine of healthy males, finds broad application in patients with inflammatory conditions such as shock, pancreatitis, and trauma. This investigation aimed to examine the impact and underlying mechanism of UTI in mice with sepsis and THP-1 cells stimulated by bacterial lipoprotein (BLP).

Modulating dendritic cells (DCs; inhibiting maturation and antigen-presenting capacity) potentially promote immune tolerance to the benefit of allografts. In this study, we aimed to elucidate the impact of miR-155 on DC maturation and allograft rejection.

Immune disorders, especially in individuals with humoral deficiencies, pose challenges during the COVID-19 pandemic. Vaccination efficacy in this population remains a critical concern amid circulating misinformation. This study aimed to analyse the post-COVID-19 vaccination immune response in individuals with immune disorders, focusing on humoral deficiency. The goal was to provide essential insights for tailored vaccination strategies.