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Tissue-resident memory T cells (TRM) comprise a newly defined subset, which comprises a major component of lymphocyte populations in diverse peripheral tissue sites, including mucosal tissues, barrier surfaces, and in other non-lymphoid and lymphoid sites in humans and mice. Many studies have focused on the role of CD8 TRM in protection; however, there is now accumulating evidence that CD4 TRM predominate in tissue sites, and are integral for in situ protective immunity, particularly in mucosal sites. New evidence suggests that mucosal CD4 TRM populations differentiate at tissue sites following the recruitment of effector T cells by local inflammation or infection. The resulting TRM populations are enriched in T-cell specificities associated with the inducing pathogen/antigen. This compartmentalization of memory T cells at specific tissue sites may provide an optimal design for future vaccination strategies. In addition, emerging evidence suggests that CD4 TRM may also play a role in immunoregulation and immunopathology, and therefore, targeting TRM may be a viable therapeutic approach to treat inflammatory diseases in mucosal sites. This review will summarize our current understanding of CD4 TRM in diverse tissues, with an emphasis on their role in protective immunity and the mechanisms by which these populations are established and maintained in diverse mucosal sites.

Asthma is a chronic inflammatory disease, which is characterized by activation of CD4+ T helper 2 cells orchestrating an allergic airway response. Whereas the role of Wnt family members in regulating T cell maintenance and maturation is established, their contribution to T cell activation in allergic asthma is not known. We hypothesized that Wnt10b plays a role in the modulation of the allergic airway response and affects T cell activation and polarization. Using an in vivo house dust mite asthma model, Wnt10b-deficient (Wnt10b−/−) mice were allergen-sensitized and inflammation, as well as T cell activation, was studied in vivo and in vitro. Wnt10b−/− mice exhibited an augmented inflammatory phenotype with an increase in eosinophils in the bronchoalveolar lavage and IL-4 and IL-13 in the lungs when compared with wild-type mice. In vitro studies confirmed an increased T helper type 2 polarization and increased T cell activation of Wnt10b−/− cells. Accordingly, the percentage of naive T cells was elevated by the addition of recombinant Wnt10b protein. Finally, Wnt10b−/− mice exhibited an increase in the percentage of effector T cells in the lungs after house dust mite sensitization, which indicated a heightened activation state, measured by an increased percentage of CD69hiCD11ahi cells. These findings suggest that Wnt10b plays an important role in regulating asthmatic airway inflammation through modification of the T cell response and is a prospective target in the disease process.

Cytokine-producing innate lymphoid cells are found at mucosal surfaces. Artis and Wherry and their colleagues show that innate 'nuocyte-like' cells accumulate in virus-infected lungs and contribute to the repair of tissues. Innate lymphoid cells (ILCs), a heterogeneous cell population, are critical in orchestrating immunity and inflammation in the intestine, but whether ILCs influence immune responses or tissue homeostasis at other mucosal sites remains poorly characterized. Here we identify a population of lung-resident ILCs in mice and humans that expressed the alloantigen Thy-1 (CD90), interleukin 2 (IL-2) receptor α-chain (CD25), IL-7 receptor α-chain (CD127) and the IL-33 receptor subunit T1-ST2. Notably, mouse ILCs accumulated in the lung after infection with influenza virus, and depletion of ILCs resulted in loss of airway epithelial integrity, diminished lung function and impaired airway remodeling. These defects were restored by administration of the lung ILC product amphiregulin. Collectively, our results demonstrate a critical role for lung ILCs in restoring airway epithelial integrity and tissue homeostasis after infection with influenza virus.

Innate lymphoid cells (ILCs), a recently identified heterogeneous cell population, are critical in orchestrating immunity and inflammation in the intestine but whether ILCs can influence immune responses or tissue homeostasis at other mucosal sites remains poorly characterized. Here we identify a population of lung-resident ILCs in mice and humans that expressed CD90, CD25, CD127 and T1-ST2. Strikingly, mouse ILCs accumulated in the lung following influenza virus infection and depletion of ILCs resulted in loss of airway epithelial integrity, decreased lung function and impaired airway remodeling. These defects could be restored by administration of the lung ILC product amphiregulin. Collectively, these results demonstrate a critical role for lung ILCs in restoring airway epithelial integrity and tissue homeostasis following influenza virus infection.

Innate lymphoid cells (ILCs), a heterogeneous cell population, are critical in orchestrating immunity and inflammation in the intestine, but whether ILCs influence immune responses or tissue homeostasis at other mucosal sites remains poorly characterized. Here we identify a population of lung-resident ILCs in mice and humans that expressed the alloantigen Thy-1 (CD90), interleukin 2 (IL-2) receptor a-chain (CD25), IL-7 receptor a-chain (CD127) and the IL-33 receptor subunit T1-ST2. Notably, mouse ILCs accumulated in the lung after infection with influenza virus, and depletion of ILCs resulted in loss of airway epithelial integrity, diminished lung function and impaired airway remodeling. These defects were restored by administration of the lung ILC product amphiregulin. Collectively, our results demonstrate a critical role for lung ILCs in restoring airway epithelial integrity and tissue homeostasis after infection with influenza virus.

Memory CD8 T cells generated by vaccines can be important for the prevention of viral infections; however, our understanding of the factors which contribute to the generation of CD8 T cell memory remains unclear. As is often the case, studying the immune response to natural infections provides valuable insight into T cell memory generation, which could then translate into the development of more effective T cell-based vaccines. To this end, we studied the kinetics and distribution of antigen presentation and the generation of a CD8 T cell response following influenza virus (IAV) and vesicular stomatitis virus (VSV) infections. The threat of new human IAV pandemics is a constant concern, which may be alleviated by the generation of broadly protective CD8 T cell-based vaccines. VSV, on the other hand, does not normally infect humans but has emerged as an extremely effective vaccine vector and could form the basis of new vaccines for diseases that are ineffectively controlled by current formulations. To study the process by which memory CD8 T cells are generated following IAV infection we tracked the recruitment and activation of naive virus specific CD8 T cells in the draining lymph nodes (dLN) of the respiratory tract. We observed early indications of antigen encounter by cells in the dLNs; however, we also observed evidence of antigen encounter within the spleen. Thus it seems that, in a model of respiratory influenza infection, virus-specific CD8 T cells are generated in both the spleen and the dLNs. Antigen presentation in the spleen may therefore serve as a mechanism to ensure the involvement of a greater proportion of the naive virus-specific CD8 T cell repertoire in the immune response to a localized infection. Furthermore, we made the novel discovery that persistent presentation of viral antigen occurs for several weeks following IAV and VSV infection. Vaccines developed to mimic this persistent antigen presentation may therefore be more effective at generating large numbers of memory CD8 T cells than current vaccine formulations.

Many clinical practice guidelines recommend similar approaches for the assessment and management of low back pain. Recommendations include use of a biopsychosocial framework to guide management with initial non-pharmacological treatment, including education that supports self-management and resumption of normal activities and exercise, and psychological programmes for those with persistent symptoms. Guidelines recommend prudent use of medication, imaging, and surgery. The recommendations are based on trials almost exclusively from high-income countries, focused mainly on treatments rather than on prevention, with limited data for cost-effectiveness. However, globally, gaps between evidence and practice exist, with limited use of recommended first-line treatments and inappropriately high use of imaging, rest, opioids, spinal injections, and surgery. Doing more of the same will not reduce back-related disability or its long-term consequences. The advances with the greatest potential are arguably those that align practice with the evidence, reduce the focus on spinal abnormalities, and ensure promotion of activity and function, including work participation. We have identified effective, promising, or emerging solutions that could offer new directions, but that need greater attention and further research to determine if they are appropriate for large-scale implementation. These potential solutions include focused strategies to implement best practice, the redesign of clinical pathways, integrated health and occupational interventions to reduce work disability, changes in compensation and disability claims policies, and public health and prevention strategies.

Low back pain is a very common symptom. It occurs in high-income, middle-income, and low-income countries and all age groups from children to the elderly population. Globally, years lived with disability caused by low back pain increased by 54% between 1990 and 2015, mainly because of population increase and ageing, with the biggest increase seen in low-income and middle-income countries. Low back pain is now the leading cause of disability worldwide. For nearly all people with low back pain, it is not possible to identify a specific nociceptive cause. Only a small proportion of people have a well understood pathological cause—eg, a vertebral fracture, malignancy, or infection. People with physically demanding jobs, physical and mental comorbidities, smokers, and obese individuals are at greatest risk of reporting low back pain. Disabling low back pain is over-represented among people with low socioeconomic status. Most people with new episodes of low back pain recover quickly; however, recurrence is common and in a small proportion of people, low back pain becomes persistent and disabling. Initial high pain intensity, psychological distress, and accompanying pain at multiple body sites increases the risk of persistent disabling low back pain. Increasing evidence shows that central pain-modulating mechanisms and pain cognitions have important roles in the development of persistent disabling low back pain. Cost, health-care use, and disability from low back pain vary substantially between countries and are influenced by local culture and social systems, as well as by beliefs about cause and effect. Disability and costs attributed to low back pain are projected to increase in coming decades, in particular in low-income and middle-income countries, where health and other systems are often fragile and not equipped to cope with this growing burden. Intensified research efforts and global initiatives are clearly needed to address the burden of low back pain as a public health problem.

The websites of prominent public health and health care organizations play pivotal roles in ensuring access to quality health information, including information guiding health equity. Several initiatives have been developed in the United States to promote equitable, fair, and inclusive health information and practices across prominent health websites. Currently, health disparities across racial groups are recognized as a critical public health problem. Simultaneously, the use of the term \"racial health equity/equities\" has been rising in academic literature. However, the definition and findability of \"racial health equity/equities\" information have not yet been evaluated in health websites. Thus, we used a systematic review approach to assess the findability and availability of racial health equity terminology and definitions across prominent health organization websites. The objective of this study was to systematically evaluate the definitions and findability of \"racial health equity/equities and related terms\" on prominent health organizations' websites. We conducted a systematic review of websites from government agencies, professional organizations, and selected health care organizations with relevance to the US health care system. Google and the US Digital Analytics program were used for initial searches. Definitions, terms, and accompanying citations for racial health equity terms, including \"racial health inequity\" or \"racial health disparities,\" were extracted from all websites. A findability tool was developed to evaluate the ease of finding the terms and definitions, with ratings ranging from \"very easy\" to \"very difficult.\" Additionally, we analyzed the themes and sentiments of the retrieved definitions. We analyzed 69 websites from prominent health organizations. Approximately half (n=31) of the websites lacked any definitions for racial health equity and related terms, and of the 38 that included definitions, most did not include citations. The definitions varied across websites, and most were rated as \"very difficult\" to find. This study highlights the absence of a systematic, standardized, and accurate approach to organizing, defining, and presenting racial health equity information on prominent health websites. Specifically, there is a lack of consistent definitions for racial health equity and related terms across prominent health organization websites.

There is currently very limited information around the spatial patterns of coral recruitment at mesophotic depths globally. This study investigated depth-related differences in coral recruitment patterns from shallow (~ 3 m) to mesophotic depths (~ 40 m) in the Indian Ocean. A new method is described for assessing coral recruitment, which allows for the improved study of recruitment patterns on deep reefs globally, as the method does not require SCUBA diving. This method allows for comparisons with other studies as there appears to be no influence on the density, composition, or settlement orientation of recruits relative to the most commonly used methods. Using this method, we investigated coral recruitment at Ningaloo Reef, Western Australia, finding the abundance of coral recruits varied significantly with depth and was highest at 25 m. The size of coral recruits changed significantly with depth, with larger recruits observed in shallower areas (3 and 8 m) than in deep areas. Distinct changes in settlement densities on tile surfaces occurred with increasing depth, with a shift to upper tile surfaces between 8 and 25 m, where the proportion of recruits increased from 10.72 to 87.69%, respectively. Overall counts of recruits were low, with minimal recruitment at the deepest sites and moderate but significant correlations between recruit numbers and hard coral cover were observed. This suggests that variations in larval supply, potentially coupled with larval behaviour and local-scale influences, limit exchange of larvae between depths and locations. This is consistent with genetic studies that show limited exchange between shallow and mesophotic reefs and points to a limited potential for mesophotic reefs to act as a source of larvae for impacted shallow reefs.