Inosine shapes PD-1 blockade responses and synergizes with dual PD-1/CTLA-4 immunotherapy to enhance antitumor immunity.

Inosine, a bacterial metabolite and agonist of the adenosine A2A receptor, modulates antitumor immunity. However, its precise effects on immune checkpoint inhibitors remain unclear. This study aimed to evaluate the impact of inosine on the efficacy of anti-programmed cell death protein 1 (PD-1) therapy and explore strategies to counteract any potential inhibitory effects.

Combination therapy with levofloxacin and the probiotic Clostridium butyricum MIYAIRI 588 enhances immune checkpoint inhibitor efficacy.

The gut microbiome influences immune checkpoint inhibitor (ICI) efficacy. In this study, we explored the effects of combined levofloxacin (LVFX) and Clostridium butyricum MIYAIRI 588 (CBM588) on ICI outcomes using a CT26 tumor model in BALB/c mice. When compared with the control, the LVFX+CBM588 combination enhanced anti-programmed cell death (PD)-1 therapy, with CD8 T cells playing a key role.

and are associated with aging of the gut microbiota and affect the efficacy of immune checkpoint inhibitors.

Introduction: The rapid increase in the number of elderly patients with cancer necessitates treatment strategies based on the effects of aging because of drastic side effects of cytotoxic anticancer agents. Immune checkpoint inhibitors (ICIs) are relatively less toxic and can be easily administered to vulnerable and aged patients suffering from cancer. The diversity of gut microbiota and specific bacteria affects the efficacy and safety of ICIs.

Ki-67 expression in anti-programmed cell death protein-1 antibody-bound CD8 T cells as a predictor of clinical benefit.

Aims: Developing predictive biomarkers for immune checkpoint inhibitors (ICIs) is important. Programmed cell death protein-1 (PD-1) receptor occupancy by anti-PD-1 antibodies on circulating T cells varies among patients. However, the association between the exhaustion of these antibody-bound T cells and the clinical efficacy of ICIs remains unknown.

Association between the gene polymorphism-determined earwax properties and external auditory canal microbiota in healthy adults.

Unlabelled: The concept of genome-microbiome interactions, in which the microenvironment determined by host genetic polymorphisms regulates the local microbiota, is important in the pathogenesis of human disease. In otolaryngology, the resident bacterial microbiota is reportedly altered in non-infectious ear diseases, such as otitis media pearls and exudative otitis media. We hypothesized that a single-nucleotide polymorphism in the ATP-binding cassette sub-family C member 11 () gene, which determines earwax properties, regulates the ear canal microbiota.

Oral administration of Bifidobacterium longum and Bifidobacterium infantis ameliorates cefcapene pivoxil-induced attenuation of anti-programmed cell death protein-1 antibody action in mice.

Gut bacteria play pivotal roles in the antitumor effects of immune checkpoint inhibitors (ICIs). However, antimicrobial therapy, often necessary for infections in cancer patients, can reduce the efficacy of ICIs. The potential of probiotics to restore ICI efficacy remains uncertain.

Isobutyric acid enhances the anti-tumour effect of anti-PD-1 antibody.

The low response rate of immune checkpoint inhibitors (ICIs) is a challenge. The efficacy of ICIs is influenced by the tumour microenvironment, which is controlled by the gut microbiota. In particular, intestinal bacteria and their metabolites, such as short chain fatty acids (SCFAs), are important regulators of cancer immunity; however, our knowledge on the effects of individual SCFAs remains limited.

and predict immune-related adverse events and efficacy of immune checkpoint inhibitor.

Introduction: Immune checkpoint inhibitors have had a major impact on cancer treatment. Gut microbiota plays a major role in the cancer microenvironment, affecting treatment response. The gut microbiota is highly individual, and varies with factors, such as age and race.

Microbiota-derived butyrate limits the autoimmune response by promoting the differentiation of follicular regulatory T cells.

Background: Rheumatoid arthritis (RA) is a chronic debilitating autoimmune disorder with a high prevalence, especially in industrialized countries. Dysbiosis of the intestinal microbiota has been observed in RA patients. For instance, new-onset untreated RA (NORA) is associated with the underrepresentation of the Clostridium cluster XIVa, including Lachnospiraceae, which are major butyrate producers, although the pathological relevance has remained obscure.