| 1. |
- Householder, John Ethan, et al.
(författare)
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One sixth of Amazonian tree diversity is dependent on river floodplains
- 2024
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Ingår i: NATURE ECOLOGY & EVOLUTION. - 2397-334X.
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Tidskriftsartikel (refereegranskat)abstract
- Amazonia's floodplain system is the largest and most biodiverse on Earth. Although forests are crucial to the ecological integrity of floodplains, our understanding of their species composition and how this may differ from surrounding forest types is still far too limited, particularly as changing inundation regimes begin to reshape floodplain tree communities and the critical ecosystem functions they underpin. Here we address this gap by taking a spatially explicit look at Amazonia-wide patterns of tree-species turnover and ecological specialization of the region's floodplain forests. We show that the majority of Amazonian tree species can inhabit floodplains, and about a sixth of Amazonian tree diversity is ecologically specialized on floodplains. The degree of specialization in floodplain communities is driven by regional flood patterns, with the most compositionally differentiated floodplain forests located centrally within the fluvial network and contingent on the most extraordinary flood magnitudes regionally. Our results provide a spatially explicit view of ecological specialization of floodplain forest communities and expose the need for whole-basin hydrological integrity to protect the Amazon's tree diversity and its function.
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| 2. |
- Luize, Bruno Garcia, et al.
(författare)
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Geography and ecology shape the phylogenetic composition of Amazonian tree communities
- 2024
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Ingår i: JOURNAL OF BIOGEOGRAPHY. - 0305-0270 .- 1365-2699.
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Tidskriftsartikel (refereegranskat)abstract
- Aim: Amazonia hosts more tree species from numerous evolutionary lineages, both young and ancient, than any other biogeographic region. Previous studies have shown that tree lineages colonized multiple edaphic environments and dispersed widely across Amazonia, leading to a hypothesis, which we test, that lineages should not be strongly associated with either geographic regions or edaphic forest types. Location: Amazonia. Taxon: Angiosperms (Magnoliids; Monocots; Eudicots). Methods: Data for the abundance of 5082 tree species in 1989 plots were combined with a mega-phylogeny. We applied evolutionary ordination to assess how phylogenetic composition varies across Amazonia. We used variation partitioning and Moran's eigenvector maps (MEM) to test and quantify the separate and joint contributions of spatial and environmental variables to explain the phylogenetic composition of plots. We tested the indicator value of lineages for geographic regions and edaphic forest types and mapped associations onto the phylogeny. Results: In the terra firme and v & aacute;rzea forest types, the phylogenetic composition varies by geographic region, but the igap & oacute; and white-sand forest types retain a unique evolutionary signature regardless of region. Overall, we find that soil chemistry, climate and topography explain 24% of the variation in phylogenetic composition, with 79% of that variation being spatially structured (R-2 = 19% overall for combined spatial/environmental effects). The phylogenetic composition also shows substantial spatial patterns not related to the environmental variables we quantified (R-2 = 28%). A greater number of lineages were significant indicators of geographic regions than forest types. Main Conclusion: Numerous tree lineages, including some ancient ones (>66 Ma), show strong associations with geographic regions and edaphic forest types of Amazonia. This shows that specialization in specific edaphic environments has played a long-standing role in the evolutionary assembly of Amazonian forests. Furthermore, many lineages, even those that have dispersed across Amazonia, dominate within a specific region, likely because of phylogenetically conserved niches for environmental conditions that are prevalent within regions.
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| 3. |
- ter Steege, Hans, et al.
(författare)
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Mapping density, diversity and species-richness of the Amazon tree flora
- 2023
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Ingår i: COMMUNICATIONS BIOLOGY. - 2399-3642. ; 6:1
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Tidskriftsartikel (refereegranskat)abstract
- Using 2.046 botanically-inventoried tree plots across the largest tropical forest on Earth, we mapped tree species-diversity and tree species-richness at 0.1-degree resolution, and investigated drivers for diversity and richness. Using only location, stratified by forest type, as predictor, our spatial model, to the best of our knowledge, provides the most accurate map of tree diversity in Amazonia to date, explaining approximately 70% of the tree diversity and species-richness. Large soil-forest combinations determine a significant percentage of the variation in tree species-richness and tree alpha-diversity in Amazonian forest-plots. We suggest that the size and fragmentation of these systems drive their large-scale diversity patterns and hence local diversity. A model not using location but cumulative water deficit, tree density, and temperature seasonality explains 47% of the tree species-richness in the terra-firme forest in Amazonia. Over large areas across Amazonia, residuals of this relationship are small and poorly spatially structured, suggesting that much of the residual variation may be local. The Guyana Shield area has consistently negative residuals, showing that this area has lower tree species-richness than expected by our models. We provide extensive plot meta-data, including tree density, tree alpha-diversity and tree species-richness results and gridded maps at 0.1-degree resolution. A study mapping the tree species richness in Amazonian forests shows that soil type exerts a strong effect on species richness, probably caused by the areas of these forest types. Cumulative water deficit, tree density and temperature seasonality affect species richness at a regional scale.
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| 4. |
- Bernal, Ximena E., et al.
(författare)
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Empowering Latina scientists
- 2019
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Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 363:6429, s. 825-826
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 5. |
- Coelho, Ana do Carmo Oliveira
(författare)
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Oxidative regulation of NCF1 in B cells and mouse models of arthritis
- 2023
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Autoimmune diseases (ADs) are chronic pathologies that result from a dysregulation of autoreactive B and T cells leading to autoantibody production and ultimately destruction of self. In paper I, we studied inflammation associated with autoimmunity. The glycolipid alpha- galactosylceramide (αGalCer) has been used as an adjuvant for vaccines, cancer treatment, and autoimmunity regulation, and shown to be effective. We show that when combined with a sterile mouse model of inflammation by injecting the pro-inflammatory cytokine IL-18, invariant natural killer T cells (iNKT) promote the expansion of autoreactive B cells instead of regulating them. This study offers insight into the usage of αGalCer in the context of chronic inflammation and implications in autoimmunity. Identifying genetic polymorphisms in autoimmune diseases is crucial for understanding how the immune system operates to find innovative therapies to treat human diseases. Genetic mapping of quantitative trait loci (QTL) and differentially expressed genes (DEGs) are helpful tools, however, the identification of single nucleotide polymorphisms (SNPs) is a difficult task. One of the major SNP associated with autoimmune arthritis was identified in rat models, using pristane-induced arthritis (PIA). An amino acid replacement in the NCF1 protein at position 153 from threonine to methionine (T153M) decreased the oxidative burst capacity of the cells, which led to increased arthritis severity. The NOX2 complex and its subunits are expressed in many cell types, predominantly in phagocytes (neutrophils and macrophages) but also in antigen-presenting cells (APCs). This complex is essential to produce reactive oxygen species (ROS). Several studies have pinpointed an association of SNPs in different subunits of the NOX2 complex with different autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), confirming the findings in animal models. The fact that a lower ROS response was associated with arthritis severity contradicts the prevailing dogma that ROS are detrimental, making it important to explain how ROS can shape and protect against autoimmunity. In paper II, we found that a point mutation in the NCF4 subunit of the NOX2 complex, has an effect in murine models of arthritis, shaping B cell responses and consequently plasma cells that are attracted to the sites of inflammation such as the synovium, secreting pathogenic antibodies that contribute to disease progression. In papers III and IV, we focused on the role of NCF1 in B cells and germinal center B cells (GC-B), respectively. Using conditional mice flipping Ncf1 alleles, we show that ROS regulates the activation and differentiation of B cells, with profound effects on T cells. Generally, mice expressing the low ROS allele (NCF1153M) exclusively in B or GC-B cells have reduced ROS levels and increased arthritis severity as compared to littermate controls harboring the high ROS allele (NCF1T153). In parallel, sera levels of anti-collagen type II (COL2) antibodies were increased in the NCF1153M mice. T cell responses were affected in both models, with increased pro-inflammatory cytokines release, immune shaping of regulatory T cells, and T follicular helper (Tfh) cells. These findings provide evidence on the pleiotropic activity of NCF1-restricted ROS and present a previously undisclosed role of NCF1 in regulating B and GC-B cells in autoimmune diseases (ADs). It is well known that B or T cells that react against self-antigens are deleted or inactivated by central tolerance mechanisms in the primary lymphoid organs bone marrow (BM) or thymus, however, some autoreactive clones can escape to the periphery and instigate ADs. In paper V, we studied antigen-specific B cells that opposite to what has been postulated are positively selected in the BM and found in the periphery of mice, rats, and even humans. These cells instead of causing autoimmunity, prevent it. COL2-transgenic mouse models do not develop spontaneous arthritis but are instead protected, mainly by the induction of regulatory T cells.
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| 6. |
- Romero-Castillo, Laura, et al.
(författare)
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Human MHC Class II and Invariant Chain Knock-in Mice Mimic Rheumatoid Arthritis with Allele Restriction in Immune Response and Arthritis Association
- 2024
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Ingår i: Advanced Science. - 2198-3844.
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Tidskriftsartikel (refereegranskat)abstract
- Transgenic mice expressing human major histocompatibility complex class II (MHCII) risk alleles are widely used in autoimmune disease research, but limitations arise due to non-physiologic expression. To address this, physiologically relevant mouse models are established via knock-in technology to explore the role of MHCII in diseases like rheumatoid arthritis. The gene sequences encoding the ectodomains are replaced with the human DRB1*04:01 and 04:02 alleles, DRA, and CD74 (invariant chain) in C57BL/6N mice. The collagen type II (Col2a1) gene is modified to mimic human COL2. Importantly, DRB1*04:01 knock-in mice display physiologic expression of human MHCII also on thymic epithelial cells, in contrast to DRB1*04:01 transgenic mice. Humanization of the invariant chain enhances MHCII expression on thymic epithelial cells, increases mature B cell numbers in spleen, and improves antigen presentation. To validate its functionality, the collagen-induced arthritis (CIA) model is used, where DRB1*04:01 expression led to a higher susceptibility to arthritis, as compared with mice expressing DRB1*04:02. In addition, the humanized T cell epitope on COL2 allows autoreactive T cell-mediated arthritis development. In conclusion, the humanized knock-in mouse faithfully expresses MHCII, confirming the DRB1*04:01 alleles role in rheumatoid arthritis and being also useful for studying MHCII-associated diseases.
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| 7. |
- Urbonaviciute, Vilma, et al.
(författare)
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Therapy targeting antigen-specific T cells by a peptide-based tolerizing vaccine against autoimmune arthritis
- 2023
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - Stockholm : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 120:25
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Tidskriftsartikel (refereegranskat)abstract
- A longstanding goal has been to find an antigen-specific preventive therapy, i.e., a vaccine, for autoimmune diseases. It has been difficult to find safe ways to steer the targeting of natural regulatory antigen. Here, we show that the administration of exog-enous mouse major histocompatibility complex class II protein bounding a unique galactosylated collagen type II (COL2) peptide (Aq-galCOL2) directly interacts with the antigen-specific TCR through a positively charged tag. This leads to expanding a VISTA-positive nonconventional regulatory T cells, resulting in a potent dominant suppressive effect and protection against arthritis in mice. The therapeutic effect is dom-inant and tissue specific as the suppression can be transferred with regulatory T cells, which downregulate various autoimmune arthritis models including antibody-induced arthritis. Thus, the tolerogenic approach described here may be a promising dominant antigen-specific therapy for rheumatoid arthritis, and in principle, for autoimmune diseases in general.
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