Making science accessible for blind and low-vision people, and those with diverse needs.

The May-June 2024 issue of Immunology & Cell Biology contains an Immunology Futures Special Feature on Disability Inclusion in Science. Diverse groups do better in science, yet individuals with disabilities face barriers to accessing education and opportunities within scientific disciplines. The Monash Sensory Science program, led by Professor Jamie Rossjohn and legally blind artist in residence Dr Erica Tandori, has transformed the accessibility for those with blindness, low vision and diverse needs (BLVDN) to experience biomedical data visualization through the form of multisensory scientific communication. The Monash Sensory Science Exhibition, first hosted in 2018 with the support of Monash University and the Australian Research Council, utilizes tactile multisensory and multimodal artworks, interactive displays and multisensory science books for BLVDN participants. In this Special Feature, scientists and researchers involved in the 2023 Autoimmunity Monash Sensory Science Exhibition discuss the novel models and displays designed to improve the scientific understanding of complex autoimmune diseases including rheumatoid arthritis, lupus, celiac disease, psoriasis and type 1 diabetes. This Special Feature aims to inform the inclusive teaching of immunology and raise discussions of how to improve access to all within our scientific institutions.

The immunology ecosystem in South Africa: striking an equitable balance between fostering discovery, promoting translation and capacity building.

In the vast and diverse continent of Africa, the field of immunology holds immense significance as it navigates the complex landscape of infectious diseases and public health challenges. In this article, we speak with Professor Clive Gray, who provides powerful and valuable insights into the unique research opportunities and immunological advancements supported by Africa's unique blend of social, economic and environmental factors and also discusses the societal and cultural challenges that need to be overcome for equitable research to be achieved across the continent.

Singapore's diverse immunology landscape: interconnected research networks enabling blue sky ideas through to translation.

Singapore stands as a dynamic hub for cutting-edge immunological research and innovation. The country's vibrant research ecosystem is supported by collaborative networks across the many national medical and scientific research institutes, fostering meaningful alliances between academia and industry. In this article, we speak to Assistant Professor Jinmiao Chen from the Agency for Science, Technology, and Research (A*STAR) and Professor Nicholas Gascoigne from the National University of Singapore (NUS), Duke-NUS Medical School and Nanyang Technological University (NTU) about immunology in Singapore. Credit: Kate Forbes.

Immunology across two islands: understanding the research landscape of Aotearoa (New Zealand).

In the unique landscape of immunology research in New Zealand, this article explores the collaborative networks spanning the two main islands, through a conversation with Associate Professor Joanna Kirman and Dr Robert Weinkove. The discussions delve into their dynamic collaborations with countries such as Asia, Australia and the United States, from their laboratories at the University of Otago and the Malaghan Institute of Medical Research, respectively, provides insight into the translational research landscape of New Zealand, and the integration of Maori culture into all aspects of scientific research and clinical practise. Kirman's work in understanding immunological memory in tuberculosis and Weinkove's research in cancer immunotherapies, particularly CAR-T cells, are highlighted. The natural beauty and accessibility of New Zealand supports its research diversity.

Highlight of 2023: Virtues and vices of CD4 CAR T cells.

This article for the Highlights of 2023 Series explores recent work that suggests that targeting CD4 CAR T cells may be critical for both of these challenges.

Granulocyte Colony-Stimulating Factor is a Determinant of Severe Bronchopulmonary Dysplasia and Coincident Retinopathy.

Bronchopulmonary dysplasia (BPD), also called chronic lung disease of immaturity, afflicts approximately one third of all extremely premature infants, causing lifelong lung damage. There is no effective treatment other than supportive care. Retinopathy of prematurity (ROP), which impairs vision irreversibly, is common in BPD, suggesting a related pathogenesis. However, specific mechanisms of BPD and ROP are not known. Herein, a neonatal mouse hyperoxic model of coincident BPD and retinopathy was used to screen for candidate mediators, which revealed that granulocyte colony-stimulating factor (G-CSF), also known as colony-stimulating factor 3, was up-regulated significantly in mouse lung lavage fluid and plasma at postnatal day 14 in response to hyperoxia. Preterm infants with more severe BPD had increased plasma G-CSF. G-CSF-deficient neonatal pups showed significantly reduced alveolar simplification, normalized alveolar and airway resistance, and normalized weight gain compared with wild-type pups after hyperoxic lung injury. This was associated with a marked reduction in the intensity, and activation state, of neutrophilic and monocytic inflammation and its attendant oxidative stress response, and protection of lung endothelial cells. G-CSF deficiency also provided partial protection against ROP. The findings in this study implicate G-CSF as a pathogenic mediator of BPD and ROP, and suggest the therapeutic utility of targeting G-CSF biology to treat these conditions.

From sex to biology: the case for gender-neutral language in science education.

In our increasingly diverse society, it is important to examine the language used in scientific fields such as biology and immunology. Gender-neutral language aims to avoid gender-based assumptions and exclusionary language, promoting inclusivity and diversity, which are essential values in scientific research.

Science and sacrifice: the pioneering journey of Dora Lush.

In 1943, Australian scientist Miss Dora Lush's life was tragically cut short in her relentless pursuit of scientific knowledge. This article commemorates the 100-year anniversary of the journal, ICB, by celebrating the remarkable career of Lush, a renowned bacteriologist who achieved unparalleled success in an era when women faced formidable barriers to tertiary education and scientific recognition. Graduating with a Master of Science from the University of Melbourne in 1934, Lush's ground-breaking research in infectious diseases, conducted in collaboration with Frank Macfarlane Burnet AO at the Walter and Eliza Hall Institute (WEHI), played a pivotal role in advancing our understanding of viruses, including influenza, herpes and myxomatosis. Lush's pivotal work on influenza provided the foundational evidence to develop the influenza vaccine, a cornerstone of global public health today. Similarly, her investigation of myxoma virus in rabbits, with its potential for pest control and ecological impact, was used to instruct creation of the world's first biological control program against a mammalian pest. Tragically, Dora Lush succumbed to scrub fever in 1943, a disease she contracted during a laboratory accident. Her unwavering commitment to science led her to offer her own blood for research as she battled the infection, exemplifying her dedication to advancing knowledge even in the face of personal adversity. Lush's legacy endures through scholarships and fellowships that bear her name in Australia, fostering the careers of aspiring scientists. Her ground-breaking research and unwavering determination continue to inspire generations, reminding us of the importance of diversity in science and the enduring impact of pioneering women like Lush.

Immunologist Margaret Baird, a trailblazer in science and empowerment.

Emeritus Professor Margaret Baird forged a luminary career for her pioneering research investigating the role of dendritic cells in cancer and infectious diseases, as an inspirational lecturer at the University of Otago and a role model to many. In this article celebrating the 100-year anniversary of ICB, we discuss Margaret's career and life journey through the eyes of her family and coauthors, as we explore her many publications in ICB and beyond.

Artificial intelligence takes center stage: exploring the capabilities and implications of ChatGPT and other AI-assisted technologies in scientific research and education.

The emergence of large language models (LLMs) and assisted artificial intelligence (AI) technologies have revolutionized the way in which we interact with technology. A recent symposium at the Walter and Eliza Hall Institute explored the current practical applications of LLMs in medical research and canvassed the emerging ethical, legal and social implications for the use of AI-assisted technologies in the sciences. This paper provides an overview of the symposium's key themes and discussions delivered by diverse speakers, including early career researchers, group leaders, educators and policy-makers highlighting the opportunities and challenges that lie ahead for scientific researchers and educators as we continue to explore the potential of this cutting-edge and emerging technology.

Gender inequities in medical research funding is driving an exodus of women from Australian STEMM academia.

Universally, women are under-represented in senior academic leadership in science, technology, engineering, maths and medicine (STEMM). Successful funding outcomes are a critical point in career progression, to continue both a scientist's research but also for their retention within the STEMM workforce. A common explanation for the lower success rate of women in securing funding is that fewer women apply for funding. However, this does not adequately explain the gender inequities in funding outcomes, both in terms of fewer funded applications and also of reduced funding awarded per grant, resulting in less overall success. Gendered funding outcomes occur within academic institutions and peak funding bodies due to historical, systemic conscious and unconscious biases during peer review. As a cumulative bias over a woman's research career, this results in women being under-represented in STEMM and the loss of their contributions to medical research, reducing innovation through a lack of diverse workforces.

Type I interferon is required for T helper (Th) 2 induction by dendritic cells.

Type 2 inflammation is a defining feature of infection with parasitic worms (helminths), as well as being responsible for widespread suffering in allergies. However, the precise mechanisms involved in T helper (Th) 2 polarization by dendritic cells (DCs) are currently unclear. We have identified a previously unrecognized role for type I IFN (IFN-I) in enabling this process. An IFN-I signature was evident in DCs responding to the helminth Schistosoma mansoni or the allergen house dust mite (HDM). Further, IFN-I signaling was required for optimal DC phenotypic activation in response to helminth antigen (Ag), and efficient migration to, and localization with, T cells in the draining lymph node (dLN). Importantly, DCs generated from Ifnar1-/- mice were incapable of initiating Th2 responses in vivo These data demonstrate for the first time that the influence of IFN-I is not limited to antiviral or bacterial settings but also has a central role to play in DC initiation of Th2 responses.

Guidelines for the use of flow cytometry and cell sorting in immunological studies (second edition).

These guidelines are a consensus work of a considerable number of members of the immunology and flow cytometry community. They provide the theory and key practical aspects of flow cytometry enabling immunologists to avoid the common errors that often undermine immunological data. Notably, there are comprehensive sections of all major immune cell types with helpful Tables detailing phenotypes in murine and human cells. The latest flow cytometry techniques and applications are also described, featuring examples of the data that can be generated and, importantly, how the data can be analysed. Furthermore, there are sections detailing tips, tricks and pitfalls to avoid, all written and peer-reviewed by leading experts in the field, making this an essential research companion.

Caveolin-1 Influences LFA-1 Redistribution upon TCR Stimulation in CD8 T Cells.

TCR stimulation by peptide-MHC complexes on APCs requires precise reorganization of molecules into the area of cellular contact to form an immunological synapse from where T cell signaling is initiated. Caveolin (Cav)1, a widely expressed transmembrane protein, is involved in the regulation of membrane composition, cellular polarity and trafficking, and the organization of signal transduction pathways. The presence of Cav1 protein in T cells was identified only recently, and its function in this context is not well understood. We show that Cav1-knockout CD8 T cells have a reduction in membrane cholesterol and sphingomyelin, and upon TCR triggering they exhibit altered morphology and polarity, with reduced effector function compared with Cav1 wild-type CD8 T cells. In particular, redistribution of the ß2 integrin LFA-1 to the immunological synapse is compromised in Cav1-knockout T cells, as is the ability of LFA-1 to form high-avidity interactions with ICAM-1. Our results identify a role for Cav1 in membrane organization and ß2 integrin function in primary CD8 T cells.

Differential polarization of C-terminal Src kinase between naive and antigen-experienced CD8+ T cells.

In CD8(+) T cells, engagement of the TCR with agonist peptide:MHC molecules causes dynamic redistribution of surface molecules including the CD8 coreceptor to the immunological synapse. CD8 associates with the Src-family kinase (SFK) Lck, which, in turn, initiates the rapid tyrosine phosphorylation events that drive cellular activation. Compared with naive T cells, Ag-experienced CD8(+) T cells make shorter contacts with APC, are less dependent on costimulation, and are triggered by lower concentrations of Ag, yet the molecular basis of this more efficient response of memory T cells is not fully understood. In this article, we show differences between naive and Ag-experienced CD8(+) T cells in colocalization of the SFKs and their negative regulator, C-terminal Src kinase (Csk). In naive CD8(+) T cells, there was pronounced colocalization of SFKs and Csk at the site of TCR triggering, whereas in Ag-experienced cells, Csk displayed a bipolar distribution with a proportion of the molecules sequestered within a cytosolic area in the distal pole of the cell. The data show that there is differential redistribution of a key negative regulator away from the site of TCR engagement in Ag-experienced CD8(+) T cells, which might be associated with the more efficient responses of these cells on re-exposure to Ag.

Murine cytomegalovirus encodes a miR-27 inhibitor disguised as a target.

Individual microRNAs (miRNAs) are rapidly down-regulated during conditions of cellular activation and infection, but factors mediating miRNA turnover are poorly understood. Infection of mouse cells with murine cytomegalovirus (MCMV) induces the rapid down-regulation of an antiviral cellular miRNA, miR-27. Here, we identify a transcript produced by MCMV that binds to miR-27 and mediates its degradation. UV-crosslinking and high-throughput sequencing [CRAC (UV-crosslinking and analysis of cDNA)] identified MCMV RNA segments associated with the miRNA-binding protein Argonaute 2 (Ago2). A cluster of hits mapped to a predicted miR-27-binding site in the 3'UTR of the previously uncharacterized ORF, m169. The expression kinetics of the m169 transcript correlated with degradation of miR-27 during infection, and m169 expression inhibited miR-27 functional activity in a reporter assay. siRNA knockdown of m169 demonstrated its requirement for miR-27 degradation following infection and did not affect other host miRNAs. Substitution of the miR-27-binding site in m169 to create complementarity to a different cellular miRNA, miR-24, resulted in down-regulation of only miR-24 following infection. The m169 transcript is cytoplasmic, capped, polyadenylated, and interacts with miRNA-27 through seed pairing: characteristic features of the normal messenger RNA (mRNA) targets of miRNAs. This virus-host interaction reveals a mode of miRNA regulation in which a mRNA directs the degradation of a miRNA. We speculate that RNA-mediated miRNA degradation could be a more general viral strategy for manipulating host cells.

Corrigendum: Dynamics of host immune response development during Schistosoma mansoni infection.

[This corrects the article DOI: 10.3389/fimmu.2022.906338.].

Novel strategy for microsphere-mediated DNA transfection.

A new approach for microsphere-mediated delivery of plasmid DNA has been developed and successfully evaluated. Basic molecular biology techniques were used to linearize and functionalize plasmid DNA by aminomodification, enabling efficient conjugation to carboxy-functionalized microspheres. A T cell hybridoma line was successfully transfected as determined by the efficient expression of a biologically relevant YFP fusion protein. Moreover, our data identified microsphere-mediated delivery of plasmid DNA as a noninvasive, nontoxic, and efficient gene delivery method with the potential to be applied to transfection-resistant, nondividing primary cells, including naïve T cells.

The Influence of Innate Lymphoid Cells and Unconventional T Cells in Chronic Inflammatory Lung Disease.

The lungs are continuously subjected to environmental insults making them susceptible to infection and injury. They are protected by the respiratory epithelium, which not only serves as a physical barrier but also a reactive one that can release cytokines, chemokines, and other defense proteins in response to danger signals, and can undergo conversion to protective mucus-producing goblet cells. The lungs are also guarded by a complex network of highly specialized immune cells and their mediators to support tissue homeostasis and resolve integrity deviation. This review focuses on specialized innate-like lymphocytes present in the lung that act as key sensors of lung insults and direct the pulmonary immune response. Included amongst these tissue-resident lymphocytes are innate lymphoid cells (ILCs), which are classified into five distinct subsets (natural killer, ILC1, ILC2, ILC3, lymphoid tissue-inducer cells), and unconventional T cells including natural killer T (NKT) cells, mucosal-associated invariant T (MAIT) cells, and γδ-T cells. While ILCs and unconventional T cells together comprise only a small proportion of the total immune cells in the lung, they have been found to promote lung homeostasis and are emerging as contributors to a variety of chronic lung diseases including pulmonary fibrosis, allergic airway inflammation, and chronic obstructive pulmonary disease (COPD). A particularly intriguing trait of ILCs that has recently emerged is their plasticity and ability to alter their gene expression profiles and adapt their function in response to environmental cues. The malleable nature of these cells may aid in rapid responses to pathogen but may also have downstream pathological consequences. The role of ILC2s in Th2 allergic airway responses is becoming apparent but the contribution of other ILCs and unconventional T cells during chronic lung inflammation is poorly described. This review presents an overview of our current understanding of the involvement of ILCs and unconventional T cells in chronic pulmonary diseases.