ERA5-based global meteorological wildfire danger maps.

Forest fires are an integral part of the natural Earth system dynamics, however they are becoming more devastating and less predictable as anthropogenic climate change exacerbates their impacts. In order to advance fire science, fire danger reanalysis products can be used as proxy for fire weather observations with the advantage of being homogeneously distributed both in space and time. This manuscript describes a reanalysis dataset of fire danger indices based on the Canadian Fire Weather Index system and the ECMWF ERA5 reanalysis dataset, which supersedes the previous dataset based on ERA-Interim.

Mice Deficient in T-bet Form Inducible NO Synthase-Positive Granulomas That Fail to Constrain .

Clearance of intracellular infections caused by Typhimurium (STm) requires IFN-γ and the Th1-associated transcription factor T-bet. Nevertheless, whereas IFN-γ mice succumb rapidly to STm infections, T-bet mice do not. In this study, we assess the anatomy of immune responses and the relationship with bacterial localization in the spleens and livers of STm-infected IFN-γ and T-bet mice.

Key data from the 17th International Workshop on Co-morbidities and Adverse Drug Reactions in HIV.

Combination antiretroviral therapy (cART) has significantly reduced HIV-related morbidity and mortality; however, residual inflammation often persists in the absence of detectable viral load. In addition, chronic use of cART and an ageing HIV-positive population present new challenges to treating physicians who must balance the need for good virological control with risk of treatment-related toxicities. Discussions at the 17th International Workshop on Co-morbidities and Adverse Drug Reactions in HIV once again sought a better understanding of the complex relationship between HIV-, treatment- and age-related factors in the development of comorbidities in those infected with HIV.

Resolving Salmonella infection reveals dynamic and persisting changes in murine bone marrow progenitor cell phenotype and function.

The generation of immune cells from BM precursors is a carefully regulated process. This is essential to limit the potential for oncogenesis and autoimmunity yet protect against infection. How infection modulates this is unclear.

Systemic flagellin immunization stimulates mucosal CD103+ dendritic cells and drives Foxp3+ regulatory T cell and IgA responses in the mesenteric lymph node.

Mucosal immunity is poorly activated after systemic immunization with protein Ags. Nevertheless, induction of mucosal immunity in such a manner would be an attractive and simple way to overcome the intrinsic difficulties in delivering Ag to such sites. Flagellin from Salmonella enterica serovar Typhimurium (FliC) can impact markedly on host immunity, in part via its recognition by TLR5.

CD8 T cells induce T-bet-dependent migration toward CXCR3 ligands by differentiated B cells produced during responses to alum-protein vaccines.

Antibody-forming cells (AFCs) expressing the chemokine receptor CXCR3 are recruited to sites of inflammation where they help clear pathogens but may participate in autoimmune diseases. Here we identify a mechanism that induces CXCR3 expression by AFC and germinal center (GC) B cells. This happens when CD8 T cells are recruited into CD4 T cell-dependent B-cell responses.

Thymic function is maintained during Salmonella-induced atrophy and recovery.

Thymic atrophy is a frequent consequence of infection with bacteria, viruses, and parasites and is considered a common virulence trait between pathogens. Multiple reasons have been proposed to explain this atrophy, including premature egress of immature thymocytes, increased apoptosis, or thymic shutdown to prevent tolerance to the pathogen from developing. The severe loss in thymic cell number can reflect an equally dramatic reduction in thymic output, potentially reducing peripheral T cell numbers.

CD31 is required on CD4+ T cells to promote T cell survival during Salmonella infection.

Hematopoietic cells constitutively express CD31/PECAM1, a signaling adhesion receptor associated with controlling responses to inflammatory stimuli. Although expressed on CD4(+) T cells, its function on these cells is unclear. To address this, we have used a model of systemic Salmonella infection that induces high levels of T cell activation and depends on CD4(+) T cells for resolution.

T-zone localized monocyte-derived dendritic cells promote Th1 priming to Salmonella.

Control of intracellular Salmonella infection requires Th1 priming and IFN-γ production. Here, we show that efficient Th1 priming after Salmonella infection requires CD11c(+) CD11b(hi) F4/80(+) monocyte-derived dendritic cells (moDCs). In non-infected spleens, moDCs are absent from T-cell zones (T zones) of secondary lymphoid tissues, but by 24 h post-infection moDCs are readily discernible in these sites.

IFN-{gamma} produced by CD8 T cells induces T-bet-dependent and -independent class switching in B cells in responses to alum-precipitated protein vaccine.

Alum-precipitated protein (alum protein) vaccines elicit long-lasting neutralizing antibody responses that prevent bacterial exotoxins and viruses from entering cells. Typically, these vaccines induce CD4 T cells to become T helper 2 (Th2) cells that induce Ig class switching to IgG1. We now report that CD8 T cells also respond to alum proteins, proliferating extensively and producing IFN-γ, a key Th1 cytokine.

The porin OmpD from nontyphoidal Salmonella is a key target for a protective B1b cell antibody response.

Invasive nontyphoidal Salmonella (NTS), including Salmonella typhimurium (STm), are major yet poorly-recognized killers of infants in sub-Saharan Africa. Death in these children is usually associated with bacteremia, commonly in the absence of gastrointestinal symptoms. Evidence from humans and animal studies suggest that severe infection and bacteremia occur when specific Ab is lacking.