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While breast cancer treatments have advanced significantly nowadays, yet metastatic, especially triple-negative breast cancer (TNBC), remains challenging with lowsurvival. Cancer immunotherapy, a promising approach for HER2-positive and TNBC, still faces resistance hurdles. Recently, numerous studies have set their sights on the resistance of immunotherapy for breast cancer. Our study provides a thorough comprehension of the current research landscape, hotspots, and emerging breakthroughs in this critical area through a meticulous bibliometric analysis. As of March 26, 2024, a total of 1341 articles on immunology resistance in breast cancer have been gathered from Web of Science Core Collection, including 765 articles and 576 reviews. Bibliometrix, CiteSpace and VOSviewer softwarewere utilized to examine publications and citations per year, prolific countries, contributive institutions, high-level journals and scholars, as well as highly cited articles, references and keywords. The research of immunotherapy resistance in breast cancer has witnessed a remarkable surge over the past seven years. The United States and China have made significant contributions, with HarvardMedical School being the most prolific institution and actively engaging in collaborations. The most contributive author is Curigliano, G from the European Institute of Oncology in Italy, while Wucherpfennig, K. W. from the Dana-Farber Cancer Institute in the USA, had the highest citations. Journals highly productive primarily focus on clinical, immunology and oncology research. Common keywords include "resistance", "expression", "tumor microenvironment", "cancer", "T cell", "therapy", "chemotherapy" and "cell". Current research endeavors to unravel the mechanisms of immune resistance in breast cancer through the integration of bioinformatics, basic experiments, and clinical trials. Efforts are underway to develop strategies that improve the effectiveness of immunotherapy, including the exploration of combination therapies and advancements in drug delivery systems. Additionally, there is a strong focus on identifying novel biomarkers that can predict patient response to immunology. This study will provide researchers with an up-to-date overview of the present knowledge in drug resistance of immunology for breast cancer, serving as a valuable resource for informed decision-making and further research on innovative approaches to address immunotherapy resistance. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD) is one of the intractable diseases. Nutritional components associated with IBD have been identified, and it is known that excessive methionine intake exacerbates inflammation, and that tryptophan metabolism is involved in inflammation. Analysis of the gut microbiota has also progressed, where Lactobacillus regulate immune cells in the intestine and suppress inflammation. However, whether the methionine and tryptophan metabolic pathways affect the growth of intestinal Lactobacillus is unknown. Here we show how transient methionine, tryptophan, and niacin deficiency affects the host and gut microbiota in mouse models of colitis (induced by dextran sodium sulfate) fed a methionine‐deficient diet (1K), tryptophan and niacin‐deficient diet (2K), or methionine, tryptophan, and niacin‐deficient diet (3K). These diets induced body weight decrease and 16S rRNA analysis of mouse feces revealed the alterations in the gut microbiota, leading to a dramatic increase in the proportion of Lactobacillus in mice. Intestinal RNA sequencing data confirmed that the expression of several serine proteases and fat‐metabolizing enzymes were elevated in mice fed with methionine, tryptophan, and niacin (MTN) deficient diet. In addition, one‐carbon metabolism and peroxisome proliferator‐activated receptor (PPAR) pathway activation were also induced with MTN deficiency. Furthermore, changes in the expression of various immune‐related cytokines were observed. These results indicate that methionine, tryptophan, and niacin metabolisms are important for the composition of intestinal bacteria and host immunity. Taken together, MTN deficiencies may serve as a Great Reset of gut microbiota and host gene expression to return to good health. [ABSTRACT FROM AUTHOR]