Reciprocal regulation of T follicular helper cells and dendritic cells drives colitis development.

The immunological mechanisms underlying chronic colitis are poorly understood. T follicular helper (T) cells are critical in helping B cells during germinal center reactions. In a T cell transfer colitis model, a lymphoid structure composed of mature dendritic cells (DCs) and T cells was found within T cell zones of colonic lymphoid follicles.

NR4A1 transcriptionally regulates the differentiation of stem-like CD8 T cells in the tumor microenvironment.

CD8 T cells are rendered exhausted in tumor and chronic infection. Among heterogeneous exhausted T cells, a subpopulation of progenitor-like (Tpex) cells have been found important for long-term tumor or pathogen control and are also the main responders in immunotherapy. Using an RFP reporter mouse for the orphan nuclear receptor NR4A1, originally characterized as critical in T cell dysfunction, we discover that the reporter is highly expressed in Tpex cells in tumor and chronic infection.

The impact of chronic disease diagnoses on smoking behavior change and maintenance: Evidence from China.

Introduction: Managing chronic diseases and tobacco use is a formidable challenge in low- and middle-income countries (LMICs) with limited health literacy and access to quality healthcare. This study examines the empirical evidence from China, utilizing quasi-experimental approaches to assess the causal effect of chronic disease diagnoses on smoking behavior.

Methods: Employing the diagnosis of chronic disease in the older cohorts of the population as a natural experiment, this study utilizes recent advancements in difference-in-difference estimation methods (CS-DID) to investigate the effect of a diagnosis on smoking behavior.

BCL6 promotes a stem-like CD8 T cell program in cancer via antagonizing BLIMP1.

Overcoming CD8 T cell exhaustion is critical in cancer immunotherapy. Recently, an intratumor stem/progenitor-like CD8 T cell (T cell) population that mediates the persistence of antitumor responses has been defined, which can further develop into a terminally differentiated CD8 T cell (T cell) subpopulation with potent cytotoxic functions. T cells are the main responders to immune checkpoint blockade therapies, yet how extrinsic signals via transcription factors control T cell generation and persistence in tumors is unclear.

Innate and adaptive immune abnormalities underlying autoimmune diseases: the genetic connections.

With the exception of an extremely small number of cases caused by single gene mutations, most autoimmune diseases result from the complex interplay between environmental and genetic factors. In a nutshell, etiology of the common autoimmune disorders is unknown in spite of progress elucidating certain effector cells and molecules responsible for pathologies associated with inflammatory and tissue damage. In recent years, population genetics approaches have greatly enriched our knowledge regarding genetic susceptibility of autoimmunity, providing us with a window of opportunities to comprehensively re-examine autoimmunity-associated genes and possible pathways.

STAT3 regulates CD8+ T cell differentiation and functions in cancer and acute infection.

In cancer, persistent antigens drive CD8+ T cell differentiation into exhausted progenitor (Texprog) and terminally exhausted (Texterm) cells. However, how the extrinsic and intrinsic regulatory mechanisms cooperate during this process still remains not well understood. Here, we found that STAT3 signaling plays essential roles in promoting intratumor Texterm cell development by enhancing their effector functions and survival, which results in better tumor control.

RORγt expression in mature T17 cells safeguards their lineage specification by inhibiting conversion to T2 cells.

RORγt is the lineage-specific transcription factor for T helper 17 (T17) cells and an attractive drug target for treating T17-associated diseases. Although the critical role of RORγt in early T17 cell differentiation has been well recognized, its function in mature T17 cell maintenance remains largely unknown. Here, we show that genetic deletion of in mature T17 cells inhibited their pathogenic functions.

Measuring Multidimensional Health Poverty in China.

This article defines the concept of "multidimensional health poverty," considering both the monetary aspects and multidimensional health deprivation of health poverty. Moreover, we set up the multidimensional health poverty index (MHPI) to measure health poverty in China by revising the traditional A-F MPI method, specifically we use the Catastrophic Health Expenditure (CHE) as a sufficient condition and income poverty as a necessary condition, and take physical, mental, and social health into account. The measurement result evidences that physical health, monetary dimensions (CHE and income poverty), and mental health contribute most to health poverty in China.

RORα is critical for mTORC1 activity in T cell-mediated colitis.

Inflammatory bowel disease (IBD) is multi-factorial chronic intestinal inflammation driven by pathogenic T cells, among which a large portion of patients are resistant to current anti-inflammatory regimes. The mechanisms underlying colitis pathogenicity and drug resistance are not fully understood. Here, we demonstrate that RORα is highly expressed in active UC patients, particularly in those non-responsive to anti-TNF treatment.

T Follicular Helper Cells Regulate Humoral Response for Host Protection against Intestinal Infection.

colonizes at the colon and causes mucosal inflammation in mice. Previous studies have revealed the importance of the innate and adaptive immune response for controlling infection. In the present study, we examined the role of T follicular helper (Tfh) cells in intestinal infection using mice with deficiency in T cells.

Antidiabetic and Neuroprotective Effect of the N-Butanol Extract of Schlecht. in STZ-Induced Diabetic Mice.

Diabetes has been associated with neurodegenerative disorders that are accompanied by memory loss and cognitive impairments, but there is no effective treatment for it at present. Schlecht. (FNS), a well-known Chinese materia medica, has been traditionally used for the folkloric treatment of diabetes and other diseases.

Regulation of Pathogenic T Helper 17 Cell Differentiation by Steroid Receptor Coactivator-3.

T helper 17 (Th17) cell development is programmed by the orphan nuclear receptor RORγt, but the underlying mechanism is not well understood. Nuclear receptor-mediated transcriptional activation depends on coactivators. Here, we show that steroid receptor coactivator-3 (SRC-3) critically regulates Th17 cell differentiation.

XRCC1 and XPD genetic polymorphisms and susceptibility to age-related cataract: a meta-analysis.

Objective: This meta-analysis aimed to determine the relationships between XRCC1 Arg399Gln (rs25487 G>A) and XPD Lys751Gln (rs1052559 A>C) polymorphisms and susceptibility to age-related cataract.

Methods: Medline (1966-2013), the Cochrane Library Database (Issue 12, 2013), EMBASE (1980-2013), CINAHL (1982-2013), Web of Science (1945-2013) and the Chinese Biomedical Database (CBM; 1982-2013) were searched without language restrictions. Various combinations of the keywords and MeSH terms were used to screen for potentially relevant studies, specifically "genetic polymorphisms" or "SNPs" or "variation" or "single nucleotide polymorphism" or "polymorphism" or "mutation" or "variant"; "X-ray repair cross complementing protein 1" or "Xeroderma Pigmentosum Group D Protein" or "X-ray repair cross complementing protein 1" or "Xeroderma Pigmentosum Group D Protein" or "XPD" or "Xeroderma Pigmentosum Complementation Group D Protein" or "ERCC2" or "XRCC1" or "XRCC1 DNA repair protein"; and "Cataract" or " Membranous Cataract" or " Pseudoaphakia.