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Objective and design This double-blind cross-over study compared the potential of bilastine, cetirizine, and fexofenadine to relieve the symptoms of allergic rhinitis. Subjects and methods Seventy-five allergic volunteers were challenged with grass pollen in the Vienna Challenge Chamber (VCC) on two consecutive days of allergen provocation; 6 h on day 1 and 4 h day 2. Bilastine 20 mg, cetirizine 10 mg, fexofenadine 120 mg, or placebo were taken orally 2 h after the start of provocation on day 1 only. Total nasal symptom scores, the global symptom scores, nasal secretions, and eye symptoms were assessed on both day 1 and day 2. Results and conclusions Bilastine had a rapid onset of action, within 1 h, and a long duration of action, greater than 26 h. Cetirizine was similar. Fexofenadine was similar on day 1 but less effective on day 2, indicating a shorter duration of action. Bilastine, like cetirizine and fexofenadine, was safe and well tolerated in this study.

Balanced immune responses in the eyes are crucial to preserve vision. The ocular immune system has long been considered distinct, owing to the so-called ‘immune privilege’ of its component tissues. More recently, intravital imaging and transcriptomic techniques have reshaped scientific understanding of the ocular immune landscape, such as revealing the specialization of immune cell populations in the various tissues of the eye. As knowledge of the phenotypes of corneal and retinal immune cells has evolved, links to both the systemic immune system, and the central and peripheral nervous systems, have been identified. Using intravital imaging, T cells have recently been found to reside in, and actively patrol, the healthy human cornea. Disease-associated retinal microglia with links to retinal degeneration have also been identified. This Review provides an updated guide to the ocular immune system, highlighting current knowledge of the immune cells that are present in steady-state and specific diseased ocular tissues, as well as evidence for their relationship to systemic disease. In addition, we discuss emerging intravital imaging techniques that can be used to visualize immune cell morphology and dynamics in living human eyes and how these could be applied to advance understanding of the human immune system.This Review provides an overview of the immune system of the eye at steady state and in ocular disease, and it describes the links between ocular immunology and systemic disease. It highlights the intravital imaging techniques that have provided insights into immune cell morphology and dynamics in living human eyes.

► The yearly incidence of oculorespiratory syndrome is variable and influenced by the specific influenza vaccine administered. ► In this analysis, the oculorespiratory syndrome incidence following influenza vaccine was reduced in HIV compared to the general population. ► The mechanism by which HIV may influence oculorespiratory syndrome pathogenesis remains unknown. Clinical experience suggests Oculorespiratory Syndrome (ORS) following influenza vaccination is rare in HIV but this is not well evaluated. We assessed ORS incidence in a randomized influenza vaccine trial of HIV participants. The overall incidence was 0.8% suggesting that influenza vaccine ORS incidence is reduced in HIV.

Inflammasomes, key molecular regulators that play an important role in inflammation, consist of a central protein, an adaptor protein ASC (apoptosis speck-like protein) and a caspase-1 protein. Upon activation, caspase-1 induces maturation of cytokines such as interleukin-1β (IL-1β) and interleukin-18 (IL-18). The release of these cytokines can result in inflammation. Inflammasomes are activated by a variety of factors and their activation involves complex signalling leading to resolution of infection, but can also contribute to the pathology of inflammatory, autoimmune, and infectious diseases. The role of NLRP1, NLRP3, NLRC4 and AIM2 inflammasomes in the pathogenesis of ocular diseases such as glaucoma, age related macular degeneration (AMD), diabetic retinopathy, dry eye and infections of the eye has been established over the past decade. In experimental studies and models, inhibition of inflammasomes generally helps to reduce the inflammation associated with these eye diseases, but as yet the role of these inflammasomes in many human eye diseases is unknown. Therefore, a need exists to study and understand various aspects of inflammasomes and their contribution to the pathology of human eye diseases. The goal of this review is to discuss the role of inflammasomes in the pathology of eye diseases, scope for anti-inflammasome therapy, and current research gaps in inflammasome-related eye disease.

Atypical hemolytic uremic syndrome (aHUS) is a rare and complex disease resulting from abnormal alternative complement activation with a wide range of clinical presentations. Extra-renal manifestations of aHUS can involve many organ systems, including the peripheral and central nervous, gastrointestinal, cardiovascular, integumentary, pulmonary, as well as the eye. While some of these extra-renal manifestations occur in the acute phase of aHUS, some can also occur as long-term sequelae of unopposed complement activation. Extra-renal symptoms are observed in approximately 20% of patients with aHUS, with the incidence of specific organ system complications ranging from a few case reports to 50% of described patients. Careful monitoring for extra-renal involvement is critical in patients with aHUS, as prompt evaluation and management may decrease the risk of high morbidity and mortality associated with aHUS.

Immunopeptides have low toxicity, low immunogenicity and targeting, and broad application prospects in drug delivery and assembly, which are diverse in application strategies and drug combinations. Immunopeptides are particularly important for regulating ocular immune homeostasis, as the eye is an immune-privileged organ. Immunopeptides have advantages in adaptive immunity and innate immunity, treating eye immune-related diseases by regulating T cells, B cells, immune checkpoints, and cytokines. This article summarizes the application strategies of immunopeptides in innate immunity and adaptive immunity, including autoimmunity, infection, vaccine strategies, and tumors. Furthermore, it focuses on the mechanisms of immunopeptides in mediating ocular immunity (autoimmune diseases, inflammatory storms, and tumors). Moreover, it reviews immunopeptides’ application strategies and the therapeutic potential of immunopeptides in the eye. We expect the immune peptide to get attention in treating eye diseases and to provide a direction for eye disease immune peptide research.

The Central Nervous System (CNS), due to its unique structure and function, possesses immune privilege, which is primarily maintained through mechanisms such as the blood-brain barrier, immune cell exclusion, and neuroglial cell regulation, effectively protecting the CNS from external insults. In recent years, research has discovered the presence of functional lymphatic systems in the meninges and the posterior segment of the eye, capable of draining cerebrospinal fluid and ocular antigens to the deep cervical lymph nodes, directly connecting with the systemic immune system. This finding has revised the traditional view that the CNS lacks lymphatic circulation and has provided a new perspective for understanding CNS immune privilege. Particularly, the posterior segment of the eye shares lymphatic drainage pathways with the brain, further revealing the complex immunological connections between the two. The ocular-cerebral connected regional lymphatic system plays a key role in ocular immune surveillance and pathological links within the CNS, with its dysfunction potentially exacerbating inflammatory responses and disease progression. Moreover, this system offers new avenues for early diagnosis, immune modulation, and drug delivery in CNS diseases, demonstrating significant clinical application potential and providing a scientific basis for the diagnosis and treatment of neurodegenerative and ophthalmic diseases.

AimsDiagnosis of IgG4-related ophthalmic disease (IgG4-ROD) rests on the correlation of clinical features, serological testing and histopathology, using internationally accepted diagnostic criteria for objective interpretation; however, several mimickers of IgG4-RD overlap in clinical presentation and histopathology. We assess histopathological features in a series of presumptive IgG4-ROD cases, with emphasis on histopathological mimics and comparison of three IgG4-ROD diagnostic/classification criteria (organ-specific (OS), revised comprehensive diagnostic (RCD) and American College of Rheumatology/European Alliance of Associations for Rheumatology (ACR/EULAR) criteria).MethodsThe histopathology database was screened for cases with clinical/histopathological suspicion of IgG4-ROD. Slides were reviewed, OS, RCD and ACR/EULAR criteria were applied, and the final clinicopathological diagnosis was recorded.Results37 patients (24 females, 13 males; 19–73 years) were diagnosed as either IgG4-ROD (n=18) or non-IgG4-related disease (n=19). Non-IgG4-related disease group showed elevated serum IgG4 (55.5%), fibrosis (100%), dense lymphoplasmacytic inflammation (92.8%), with an increase in tissue IgG4+plasma cells (57.1%) and elevated IgG4:IgG+plasma cell ratio (14.3%). ACR/EULAR missed 50% (9/18, sensitivity—52.8%) of true IgG4-ROD cases, while OS and RCD criteria missed 11.1% (2/18, sensitivity—88.9%) of IgG-ROD cases. ACR/EULAR criteria mislabelled 7.14% (1/14, specificity—90.9%) while OS and RCD criteria wrongly categorised 71.4% (10/14, specificity—47.4%) and 50% (7/14, specificity—63.2%) specific non-IgG4-ROD cases as IgG4-ROD. Storiform fibrosis, obliterative phlebitis, increased IgG4:IgG+plasma cell ratio and elevated serum IgG were statistically significant in distinguishing IgG4-ROD from its mimics.ConclusionACR/EULAR criteria showed high specificity but were cumbersome and sensitivity was low, while RCD and OS criteria showed low specificity. Stringent clinicopathological correlation to exclude mimics is critical in avoiding diagnostic errors in IgG4-ROD.

Infections with the protozoan parasite Toxoplasma gondii are frequent, but one of its main consequences, ocular toxoplasmosis (OT), remains poorly understood. While its clinical description has recently attracted more attention and publications, the underlying pathophysiological mechanisms are only sparsely elucidated, which is partly due to the inherent difficulties to establish relevant animal models. Furthermore, the particularities of the ocular environment explain why the abundant knowledge on systemic toxoplasmosis cannot be just transferred to the ocular situation. However, studies undertaken in mouse models have revealed a central role of interferon gamma (IFNγ) and, more surprisingly, interleukin 17 (IL17), in ocular pathology and parasite control. These studies also show the importance of the genetic background of the infective Toxoplasma strain. Indeed, infections due to exotic strains show a completely different pathophysiology, which translates in a different clinical outcome. These elements should lead to more individualized therapy. Furthermore, the recent advance in understanding the immune response during OT paved the way to new research leads, involving immune pathways poorly studied in this particular setting, such as type I and type III interferons. In any case, deeper knowledge of the mechanisms of this pathology is needed to establish new, more targeted treatment schemes.

Ocular symptoms occur in 40% of patients with allergic rhinitis. The purpose of this study was to determine whether nasal challenge with antigen induces a nasal-ocular reflex. We performed a double-blind crossover trial in 20 subjects. A nasal challenge with antigen was performed in one nostril, and the response was assessed in both nostrils and both eyes. Subjects were treated before challenge with either placebo or azelastine, an H1-antihistamine. Nasal challenge with antigen led to a nasonasal reflex and a nasal-ocular reflex as manifested by an increase in symptoms and secretion weights. Treatment with azelastine reduced both reflexes. A nasal-ocular reflex follows nasal challenge with antigen and probably contributes to the ocular symptoms associated with allergic rhinitis.