This paper develops a new approach to band subset selection (BSS) for hyperspectral image classification (HSIC) which selects multiple bands simultaneously as a band subset, referred to as ...simultaneous multiple band selection (SMMBS), rather than one band at a time sequentially, referred to as sequential multiple band selection (SQMBS), as most traditional band selection methods do. In doing so, a criterion is particularly developed for BSS that can be used for HSIC. It is a linearly constrained minimum variance (LCMV) derived from adaptive beamforming in array signal processing which can be used to model misclassification errors as the minimum variance. To avoid an exhaustive search for all possible band subsets, two numerical algorithms, referred to as sequential (SQ) and successive (SC) algorithms are also developed for LCMV-based SMMBS, called SQ LCMV-BSS and SC LCMV-BSS. Experimental results demonstrate that LCMV-based BSS has advantages over SQMBS.
Due to advent of sensor technology, hyperspectral imaging has become an emerging technology in remote sensing. Many problems, which cannot be resolved by multispectral imaging, can now be solved by ...hyperspectral imaging. The aim of this Special Issue "Hyperspectral Imaging and Applications" is to publish new ideas and technologies to facilitate the utility of hyperspectral imaging in data exploitation and to further explore its potential in different applications. This Special Issue has accepted and published 25 papers in various areas, which can be organized into 7 categories with the number of papers published in every category included in its open parenthesis. 1. Data Unmixing (2 papers)2. Spectral variability (2 papers)3. Target Detection (3 papers)4. Hyperspectral Image Classification (6 papers)5. Band Selection (2 papers)6. Data Fusion (2 papers)7. Applications (8 papers) Under every category each paper is briefly summarized by a short description so that readers can quickly grab its content to find what they are interested in.
One fundamental task of hyperspectral imaging is spectral unmixing. In this case, the conventional pure pixel-based hyperspectral image classification (HSIC) may not work effectively for mixed ...pixels. This article presents a kernel-based approach to hyperspectral mixed pixel classification (HMPC) which includes two nonlinear mixed pixel classifiers, kernel constrained energy minimization (KCEM) and kernel linearly constrained minimum variance (KLCMV) to replace the widely used pure pixel-based support vector machine (SVM) classifier. Interestingly, what the binary-class and multiclass SVM classifiers are to pure pixel-based HSIC can be similarly derived for what a single-class KCEM detector and a multiclass KLCMV detector are to HMPC. In particular, the commonly used discrete classification map-based hard classification measures, average accuracy (AA) and overall accuracy (OA) for performance evaluation can be further generalized to real-valued mixed class abundance fractional map-based soft classification measures via 3-D receiver operating characteristic (3-D ROC) analysis-derived detection measures. Extensive experiments are conducted to demonstrate the utility of HMPC where KCEM/KLCMV not only significantly improve the classification performance of CEM/LCMV-based classifiers but also outperform many existing spectral-spatial classification methods.
Although CD4+ T cell “help” is crucial to sustain antiviral immunity, the mechanisms by which CD4+ T cells regulate CD8+ T cell differentiation during chronic infection remain elusive. Here, using ...single-cell RNA sequencing, we show that CD8+ T cells responding to chronic infection were more heterogeneous than previously appreciated. Importantly, our findings uncovered the formation of a CX3CR1-expressing CD8+ T cell subset that exhibited potent cytolytic function and was required for viral control. Notably, our data further demonstrate that formation of this cytotoxic subset was critically dependent on CD4+ T cell help via interleukin-21 (IL-21) and that exploitation of this developmental pathway could be used therapeutically to enhance the killer function of CD8+ T cells infiltrated into the tumor. These findings uncover additional molecular mechanisms of how “CD4+ T cell help” regulates CD8+ T cell differentiation during persistent infection and have implications toward optimizing the generation of protective CD8+ T cells in immunotherapy.
Display omitted
•scRNA-seq unveils a unique subset of cytolytic CD8+ T cells during chronic infection•CX3CR1+ CD8+ T cells are required to control chronic viral infection•CD4+ T cell help via IL-21 production is critical for CX3CR1+ CD8+ T cell formation•IL-21-producing CD4+ T cells enhance CX3CR1+ TIL formation and tumor control
The mechanisms by which CD4+ T cell help sustains exhausted CD8+ T cells during chronic infection have remained elusive. Here, Zander and colleagues show that CD4+ T-cell-derived IL-21 is required for the formation of a distinct subset of cytolytic CX3CR1+CD8+ T cells that protect against chronic infection and cancer.
CD4+ T cell-derived interleukin 21 (IL-21) sustains CD8+ T cell responses during chronic viral infection, but the helper subset that confers this protection remains unclear. Here, we applied scRNA ...and ATAC-seq approaches to determine the heterogeneity of IL-21+CD4+ T cells during LCMV clone 13 infection. CD4+ T cells were comprised of three transcriptionally and epigenetically distinct populations: Cxcr6+ Th1 cells, Cxcr5+ Tfh cells, and a previously unrecognized Slamf6+ memory-like (Tml) subset. T cell differentiation was specifically redirected toward the Tml subset during chronic, but not acute, LCMV infection. Although this subset displayed an enhanced capacity to accumulate and some developmental plasticity, it remained largely quiescent, which may hinder its helper potential. Conversely, mixed bone marrow chimera experiments revealed that Tfh cell-derived IL-21 was critical to sustain CD8+ T cell responses and viral control. Thus, strategies that bolster IL-21+Tfh cell responses may prove effective in enhancing CD8+ T cell-mediated immunity.
Display omitted
•scRNA-seq reveals heterogeneity among IL-21+ CD4+ T cells during chronic LCMV infection•Differential expression of CXCR6 and CXCR5 defines three distinct CD4+ T cell subsets•Chronic LCMV infection redirects CD4+ T cell differentiation toward a memory-like subset•Tfh-derived IL-21 critically sustains effector CD8+ T cell development and viral control
CD4+ T cell help via IL-21 production is critical to sustain CD8+ T cell responses during chronic viral infection, but whether a particular subset mediates this process remains unclear. Zander et al. identify heterogeneity among IL-21-producing CD4+ T cells during chronic infection and find that Tfh-derived IL-21 promotes effector CD8+ T cell development and antiviral immunity.
Virus-specific PD1+ Tcf1+ memory-like CD8+ T cells (TMLs) maintain the CD8+ T cell response during chronic viral infection. However, the fate of these cells following cessation of persistent antigen ...exposure has been unclear. Here, we find that TMLs persist upon transfer into antigen-free hosts and form memory following recall stimulation. Phenotypic, functional, and transcriptome analyses show that TML-derived memory cells resemble those arising in response to acute, resolved infection, but they retain features of chronically stimulated cells, including elevated PD-1 and Tox and reduced cytokine expression. This chronic infection imprint is largely accounted for by constitutive Tox expression. Virus-specific Tcf1+ CD8+ T cells that persist after clearance of systemic infection also display a chronic infection imprint. Notwithstanding, renewed virus exposure induces a recall response, which controls virus infection in part. Thus, cessation of chronic antigen exposure yields a memory CD8+ T cell compartment that reflects prior stimulation.
Display omitted
•PD-1+ Tcf1+ CD8+ T cells (TMLs) establish memory upon clearance of chronic infection•TML-derived memory cells globally resemble conventional memory CD8+ T cells•TML-derived memory cells retain a permanent imprint of prior chronic stimulation•Persistent Tox expression explains the chronic infection imprint in memory cells
Although memory-like PD-1+ Tcf1+ CD8+ T cells (TMLs) sustain the immune response to chronic viral infection, the fate of these cells in the absence of persistent stimulation has remained unclear. Charmoy et al. find that TMLs can yield functional memory that retains a permanent imprint of prior chronic stimulation.
Reinvigoration of exhausted CD8+ T (Tex) cells by checkpoint immunotherapy depends on the activation of precursors of exhausted T (Tpex) cells, but the local anatomical context of their maintenance, ...differentiation, and interplay with other cells is not well understood. Here, we identified transcriptionally distinct Tpex subpopulations, mapped their differentiation trajectories via transitory cellular states toward Tex cells, and localized these cell states to specific splenic niches. Conventional dendritic cells (cDCs) were critical for successful αPD-L1 therapy and were required to mediate viral control. cDC1s were dispensable for Tpex cell expansion but provided an essential niche to promote Tpex cell maintenance, preventing their overactivation and T-cell-mediated immunopathology. Mechanistically, cDC1s insulated Tpex cells via MHC-I-dependent interactions to prevent their activation within other inflammatory environments that further aggravated their exhaustion. Our findings reveal that cDC1s maintain and safeguard Tpex cells within distinct anatomical niches to balance viral control, exhaustion, and immunopathology.
Display omitted
•Determined differentiation trajectory and location of Tex cells and their precursors•cDC1s are essential for viral control but not for Tpex cell expansion•cDC1s maintain Tpex cell niches in an MHC-I-dependent manner•cDC1s limit activation-driven T cell exhaustion and immunopathology
Dähling et al. establish the role of cDCs for immunotherapy and find that cDC1s are required to mediate viral control. cDC1s provide a niche to maintain the precursors of exhausted T (Tpex) cell population and prevent their overactivation and subsequent immunopathology. These findings reveal the importance of cDC1s in maintaining Tpex cells to balance viral control, exhaustion, and immunopathology.
Chronic infections promote the terminal differentiation (or “exhaustion”) of T cells and are thought to preclude the formation of memory T cells. In contrast, we discovered a small subpopulation of ...virus-specific CD8+ T cells that sustained the T cell response during chronic infections. These cells were defined by, and depended on, the expression of the transcription factor Tcf1. Transcriptome analysis revealed that this population shared key characteristics of central memory cells but lacked an effector signature. Unlike conventional memory cells, Tcf1-expressing T cells displayed hallmarks of an “exhausted” phenotype, including the expression of inhibitory receptors such as PD-1 and Lag-3. This population was crucial for the T cell expansion that occurred in response to inhibitory receptor blockade during chronic infection. These findings identify a memory-like T cell population that sustains T cell responses and is a prime target for therapeutic interventions to improve the immune response in chronic infections.
Display omitted
•Virus-specific Tcf1+CD8+ T cells sustain the immune response to chronic infection•These cells have traits of central memory and exhausted but not of effector cells•They retain proliferative capacity, regenerate, and produce differentiated cells•They are critical for the proliferative response to inhibitory receptor blockade
Held and colleagues identify a population of Tcf1+CD8+ T cells that sustains the immune response during chronic viral infection. These cells exhibit features of central memory and exhausted T cells and expand upon inhibitory receptor blockade, presenting a prime target for therapeutic interventions to improve the immune response in chronic infections.
T cell dysfunction is a characteristic feature of chronic viral infection and cancer. Recent studies in chronic lymphocytic choriomeningitis virus (LCMV) infection have defined a PD-1+ Tcf-1+ CD8+ ...T cell subset capable of self-renewal and differentiation into more terminally differentiated cells that downregulate Tcf-1 and express additional inhibitory molecules such as Tim3. Here, we demonstrated that expression of the glycoprotein CD101 divides this terminally differentiated population into two subsets. Stem-like Tcf-1+ CD8+ T cells initially differentiated into a transitory population of CD101−Tim3+ cells that later converted into CD101+ Tim3+ cells. Recently generated CD101−Tim3+ cells proliferated in vivo, contributed to viral control, and were marked by an effector-like transcriptional signature including expression of the chemokine receptor CX3CR1, pro-inflammatory cytokines, and granzyme B. PD-1 pathway blockade increased the numbers of CD101−Tim3+ CD8+ T cells, suggesting that these newly generated transitional cells play a critical role in PD-1-based immunotherapy.
Display omitted
•CX3CR1+ CD8+ T cells are recent progeny of stem-like cells in chronic infection•CX3CR1+ cells differentiate to a dysfunctional state marked by CD101 expression•Transitory CX3CR1+ cells express effector molecules and contribute to viral control•PD-1 pathway blockade increases the number of antigen-specific transitory cells
Chronic viral infection induces exhaustion of antigen-specific T cells. Hudson and colleagues define a transitory, effector-like population of CD8+ T cells that are recently generated from stem-like CD8+ T cells in chronic infection. These transitory cells contribute to viral control and are increased in number following PD-1 pathway blockade.
The proprotein convertase subtilisin/kexins (PCSKs) regulate biological actions by cleaving immature substrate proteins. The archetype PCSK, FURIN, promotes the pathogenicity of viruses by ...proteolytically processing viral proteins. FURIN has also important regulatory functions in both innate and adaptive immune responses but its role in the CD8+ CTLs remains enigmatic. We used a T‐cell‐specific FURIN deletion in vivo to demonstrate that FURIN promotes host response against the CTL‐dependent lymphocytic choriomeningitis virus by virtue of restricting viral burden and augmenting interferon gamma (IFNG) production. We also characterized Furin KO CD8+ T cells ex vivo, including after their activation with FURIN regulating cytokines IL12 or TGFB1. Furin KO CD8+ T cells show an inherently activated phenotype characterized by the upregulation of effector genes and increased frequencies of CD44+, TNF+, and IFNG+ cells. In the activated CTLs, FURIN regulates the productions of IL2, TNF, and GZMB and the genes associated with the TGFBR‐signaling pathway. FURIN also controls the expression of Eomes, Foxo1, and Bcl6 and the levels of ITGAE and CD62L, which implies a role in the development of CTL memory. Collectively, our data suggest that the T‐cell expressed FURIN is important for host responses in viral infections, CTL homeostasis/activation, and memory development.
We demonstrate that T‐cell‐expressed FURIN is required for normal host response against the CTL‐dependent lymphocytic choriomeningitis virus (LCMV) infection. Additionally, FURIN is important in controlling the CD8+ T‐cell homeostasis/activation and memory cell development. Overall, our data suggests that FURIN regulates the biology of CD8+ T cells.
PDF
