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Background: Conservation decisions not only impact wildlife, habitat, and environmental health, but also human wellbeing and social justice. The inclusion of safeguards and equity considerations in the conservation field has increasingly garnered attention in international policy processes and amongst conservation practitioners. Yet, what constitutes an 'equitable' solution can take many forms, and how the concept is treated within conservation research is not standardized. This review explores how social equity is conceptualized and assessed in conservation research. Methods/Design: Using a structured search and screening process, we identified 138 peer-reviewed studies that addressed equity in relation to conservation actions. The authors developed a coding framework to guide the review process, focusing on the current state of, definitions used for, and means of assessing social equity in empirical conservation research. Review Results: Results show that empirical research on social equity in conservation is rapidly growing, with the majority of studies on the topic published only since 2009. Equity within conservation research is skewed toward distributional concerns and to a lesser extent procedural issues, with recognition and contextual equity receiving little attention. Studies are primarily situated in forested biomes of the Global South. Conservation interventions mostly resulted in mixed or negative impacts on equity. Synthesis and Discussion: Our results demonstrate the current limitations of research on equity in conservation, and raise challenging questions about the social impacts of conservation and how to ameliorate equity concerns. Framing of equity within conservation research would benefit from greater transparency of study motivation, more explicit definition of how equity is used within the study context, and consideration for how best to assess it. We recommend that the empirical conservation literature more deeply engage with different notions of equity when studying, planning, and implementing actions to address potential trade-offs among equity and conservation objectives and beneficiaries.

Food security, in the context of a rapidly changing climate, is one of the most prominent global challenges facing human societies today. Pacific Island Countries and Territories (PICTs) are particularly vulnerable to the adverse effects of climate change, while facing additional stress from globalisation and increased supply chain disruption. This review aims to document our understanding of food system vulnerability to climate change in the region, and identify the existing studies that could inform policy and decision-making. The review also serves to discern the dominant focal areas of research, as well as where gaps exist for emerging research.Using keyword searches on the web, scholarly databases, and targeted organisational websites, we identified 104 studies published from 2010 to 2022 that looked at the impacts of climate change on some aspect of the food system in at least one PICT. We found that the majority of empirical research on climate impacts on food systems in PICTs focused on the biophysical components of food production rather than the complex interactions between the socio-economic and biophysical factors that make up food systems. An incomplete understanding of the impacts from climate change could result in maladaptation and an undermining of food system resilience.

Antigens derived from viral infection or vaccination can persist within a host for many weeks after resolution of the infection or vaccine responses. We previously identified lymphatic endothelial cells (LEC) as the repository for this antigen archival, yet LECs are unable to present their archived antigens to CD8 + T cells, and instead transfer their antigens to CD11c + antigen-presenting cells (APC). Here we show that the exchange of archived antigens between LECs and APCs is mediated by migratory dendritic cells (DC). After vaccination, both migratory basic leucine zipper ATF-like transcription factor 3 (BatF3)-dependent and BatF3-independent DCs are responsible for antigen exchange and cross-presentation. However, exchange of archived viral antigens is mediated only by BatF3-dependent migratory DCs potentially acquiring apoptotic LECs. In conclusion, LEC-archived antigens are exchanged with migratory DCs, both directly and through LEC apoptosis, to cross-present archived antigens to circulating T cells. Viral infection and vaccination both induce lasting persistence of antigens for protective responses. Here the authors show that migratory dendritic cells, independent of the transcription factor BatF3 for their development, contribute to “archived antigen” exchange with lymphatic endothelial cells.

Many vaccines include aluminum salts (alum) as adjuvants despite little knowledge of alum’s functions. Host DNA rapidly coats injected alum. Here, we further investigated the mechanism of alum and DNA’s adjuvant function. Our data show that DNase coinjection reduces CD4 T-cell priming by i.m. injected antigen + alum. This effect is partially replicated in mice lacking stimulator of IFN genes, a mediator of cellular responses to cytoplasmic DNA. Others have shown that DNase treatment impairs dendritic cell (DC) migration from the peritoneal cavity to the draining lymph node in mice immunized i.p. with alum. However, our data show that DNase does not affect accumulation of, or expression of costimulatory proteins on, antigen-loaded DCs in lymph nodes draining injected muscles, the site by which most human vaccines are administered. DNase does inhibit prolonged T-cell–DC conjugate formation and antigen presentation between antigen-positive DCs and antigen-specific CD4 T cells following i.m. injection. Thus, from the muscle, an immunization site that does not require host DNA to promote migration of inflammatory DCs, alum acts as an adjuvant by introducing host DNA into the cytoplasm of antigen-bearing DCs, where it engages receptors that promote MHC class II presentation and better DC–T-cell interactions.

The prevention of autoimmunity requires the elimination of self-reactive T cells during their development and maturation. The expression of diverse self-antigens by stromal cells in the thymus is essential to this process and depends, in part, on the activity of the autoimmune regulator (Aire) gene. Here we report the identification of extrathymic Aire-expressing cells (eTACs) resident within the secondary lymphoid organs. These stromally derived eTACs express a diverse array of distinct self-antigens and are capable of interacting with and deleting naïve autoreactive T cells. Using two-photon microscopy, we observed stable antigen-specific interactions between eTACs and autoreactive T cells. We propose that such a secondary network of self-antigen-expressing stromal cells may help reinforce immune tolerance by preventing the maturation of autoreactive T cells that escape thymic negative selection.

Lymphocyte migration is essential for the function of the adaptive immune system, and regulation of T cell entry into tissues is an effective therapy in autoimmune diseases. Little is known about the specific role of cytoskeletal effectors that mediate mechanical forces and morphological changes essential for migration in complex environments. We developed a new Formin-like-1 (FMNL1) knock-out mouse model and determined that the cytoskeletal effector FMNL1 is selectively required for effector T cell trafficking to inflamed tissues, without affecting naïve T cell entry into secondary lymphoid organs. Here, we identify a FMNL1-dependent mechanism of actin polymerization at the back of the cell that enables migration of the rigid lymphocyte nucleus through restrictive barriers. Furthermore, FMNL1-deficiency impairs the ability of self-reactive effector T cells to induce autoimmune disease. Overall, our data suggest that FMNL1 may be a potential therapeutic target to specifically modulate T cell trafficking to inflammatory sites.

Interferons (IFNs) target macrophages to regulate inflammation and resistance to microbial infections. The type II IFN (IFNγ) acts on a cell surface receptor (IFNGR) to promote gene expression that enhance macrophage inflammatory and anti-microbial activity. Type I IFNs can dampen macrophage responsiveness to IFNγ and are associated with increased susceptibility to numerous bacterial infections. The precise mechanisms responsible for these effects remain unclear. Type I IFNs silence macrophage ifngr1 transcription and thus reduce cell surface expression of IFNGR1. To test how these events might impact macrophage activation and host resistance during bacterial infection, we developed transgenic mice that express a functional FLAG-tagged IFNGR1 (fGR1) driven by a macrophage-specific promoter. Macrophages from fGR1 mice expressed physiologic levels of cell surface IFNGR1 at steady state and responded equivalently to WT C57Bl/6 macrophages when treated with IFNγ alone. However, fGR1 macrophages retained cell surface IFNGR1 and showed enhanced responsiveness to IFNγ in the presence of type I IFNs. When fGR1 mice were infected with the bacterium Listeria monocytogenes their resistance was significantly increased, despite normal type I and II IFN production. Enhanced resistance was dependent on IFNγ and associated with increased macrophage activation and antimicrobial function. These results argue that down regulation of myeloid cell IFNGR1 is an important mechanism by which type I IFNs suppress inflammatory and anti-bacterial functions of macrophages.

Naïve T cell activation in secondary lymphoid organs such as lymph nodes (LNs) occurs upon recognition of cognate antigen presented by antigen presenting cells (APCs). T cell activation requires cytoskeleton rearrangement and sustained interactions with APCs. Enabled/vasodilator-stimulated phosphoprotein (Ena/VASP) proteins are a family of cytoskeletal effector proteins responsible for actin polymerization and are frequently found at the leading edge of motile cells. Ena/VASP proteins have been implicated in motility and adhesion in various cell types, but their role in primary T cell interstitial motility and activation has not been explored. Our goal was to determine the contribution of Ena/VASP proteins to T cell–APC interactions, T cell activation, and T cell expansion in vivo . Our results showed that naïve T cells from Ena/VASP-deficient mice have a significant reduction in antigen-specific T cell accumulation following Listeria monocytogenes infection. The kinetics of T cell expansion impairment were further confirmed in Ena/VASP-deficient T cells stimulated via dendritic cell immunization. To investigate the cause of this T cell expansion defect, we analyzed T cell–APC interactions in vivo by two-photon microscopy and observed fewer Ena/VASP-deficient naïve T cells interacting with APCs in LNs during priming. We also determined that Ena/VASP-deficient T cells formed conjugates with significantly less actin polymerization at the T cell–APC synapse, and that these conjugates were less stable than their WT counterparts. Finally, we found that Ena/VASP-deficient T cells have less LFA-1 polarized to the T cell–APC synapse. Thus, we conclude that Ena/VASP proteins contribute to T cell actin remodeling during T cell–APC interactions, which promotes the initiation of stable T cell conjugates during APC scanning. Therefore, Ena/VASP proteins are required for efficient activation and expansion of T cells in vivo .

T cells and B cells have been identified in human and murine islets, but the phenotype and role of islet lymphocytes is unknown. Resident immune populations set the stage for responses to inflammation in the islets during homeostasis and diabetes. Thus, we sought to identify the phenotype and effector function of islet lymphocytes to better understand their role in normal islets and in islets under metabolic stress. Lymphocytes were located in the islet parenchyma, and were comprised of a mix of naïve, activated, and memory T cell and B cell subsets, with an enrichment for regulatory B cell subsets. Use of a Nur77 reporter indicated that CD8 T cells and B cells both received local antigen stimulus, indicating that they responded to antigens present in the islets. Analysis of effector function showed that islet T cells and B cells produced the regulatory cytokine IL-10. The regulatory phenotype of islet T cells and B cells and their response to local antigenic stimuli remained stable under conditions of metabolic stress in the diet induced obesity (DIO) model. T cells present in human islets retained a similar activated and memory phenotype in non-diabetic and T2D donors. Under steady-state conditions, islet T cells and B cells have a regulatory phenotype, and thus may play a protective role in maintaining tissue homeostasis.

The planet is facing enduring and intersecting challenges from climate change, land degradation, habitat and biodiversity loss, as well as social inequalities. To achieve sustainability in the face of these crises, transformative changes are essential. While the path towards a more sustainable future has the capacity to bring net social benefits, it also holds the potential to exacerbate vulnerabilities. As such, there is growing recognition that social equity and justice must be central to action for sustainability transformations. However, it remains unclear what characterises a ‘just transformation’ and how to achieve it. To develop a baseline understanding of how social justice is integrated into sustainability transformations and to help guide research and practice in this emerging field, we present a systematic literature review of 125 papers that explicitly account for social equity and justice in research on place‐based transformations. Results reveal considerable variation and ambiguity in how the concepts of transformation and equity are employed, and highlight a focus on a narrow set of systems, with a large number of papers focusing on energy and urban transformations, located primarily in the Global North. While distributional and procedural dimensions of justice are frequently addressed, contextual and restorative justice remain underexplored. We identify key areas that require future attention in research and practice, including promoting interdisciplinary research that champions global inclusivity as well as a more explicit consideration of contextual justice and place. Short The planet faces complex and interconnected challenges such as climate change, biodiversity loss, and social inequalities, necessitating transformative change for sustainability. This paper presents a systematic review of research on sustainability transformations reveals significant variation in how justice and equity are addressed, with a narrow focus on certain regions and aspects of justice. To achieve a truly just transformation, future research must prioritise global inclusivity and place greater emphasis on equitable processes, particularly in relation to contextual and restorative justice.