Immunoglobulins in tear in trachoma patients.

Dk, Sen; Sarin, G. S.; Saha, Kunal

doi:10.1136/bjo.61.3.218

Cited by 9 publications

(4 citation statements)

References 5 publications

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“…The apparently high levels of IgG in the sclera are presumably derived from the tear IgG leaked into orbit. [58][59][60][61] Similarly, the surprisingly high levels of IgG in the avascular cornea must come either via the aqueous from the epithelium of the ciliary processes 62 or from the tear film. The label in these regions is unlikely to be nonspecific because it was not present after pre-absorption with IgG.…”

Section: Normal Igg Distributionmentioning

confidence: 99%

Localization of IgG in the normal and dystrophic rat retina after laser lesions*

Chu¹,

Alder²,

Humphrey³

et al. 1999

Australian and New Zealand Journal of Ophthalmology

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Section: Normal Igg Distributionmentioning

confidence: 99%

Localization of IgG in the normal and dystrophic rat retina after laser lesions*

Chu¹,

Alder²,

Humphrey³

et al. 1999

Australian and New Zealand Journal of Ophthalmology

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“…In our results, a positive correlation was observed between clinical signs and B lymphocytes infiltrate (r coefficient = 0.52, p = 0.00032). A 1977 study on immunoglobulins in trachoma patients’ tears observed a lower quantity of IgA in trachoma cases than in healthy patients (without significant differences between trachoma phases) [35]. However, Taylor et al ., in a Cynomolgus model of trachoma, although using another Ct strain (E/Bour), found a delayed increase in tear IgA after conjunctival Ct exposure, and persistence of systemic IgG [23], consistent with our findings.…”

Section: Discussionmentioning

confidence: 99%

Multimodal mucosal and systemic immune characterization of a novel non-human primate trachoma model highlights the critical role of local immunity during acute phase disease

Paulet,

Contreras,

Galhaut

et al. 2023

Preprint

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BackgroundTrachoma -the leading cause of blindness worldwide as a result of infection-is caused by repeatedChlamydia trachomatis(Ct) conjunctival infections. Disease develops in two phases: i) active (acute trachoma, characterized by follicular conjunctivitis), then long-term ii) scarring (chronic trachoma, characterized by conjunctival fibrosis, corneal opacification and eyelid malposition). Scarring trachoma is driven by the number and the severity of reinfections. The immune system is a pivotal aspect of disease, involved in disease aggravation, but also key for exploitation in development of a trachoma vaccine. Therefore, we characterized clinical and local immune response kinetics in a non-human primate model of acute conjunctival Ct infection and disease.Methodology/Principal FindingsThe conjunctiva of non-human primate (NHP, Cynomolgus monkeys -Macaca fascicularis-) were inoculated with Ct (B/Tunis-864 strain, B serovar). Clinical ocular monitoring was performed using a standardized photographic grading system, and local immune responses were assessed using multi-parameter flow cytometry of conjunctival cells, tear fluid cytokines, immunoglobulins, and Ct quantification. Clinical findings were similar to those observed during acute trachoma in humans, with the development of typical follicular conjunctivitis from the 4thweek post-exposure to the 11thweek. Immunologic analysis revealed an early phase influx of T cells in the conjunctiva and elevated interleukins 4, 8, and 5, before a later phase monocytic influx accompanied by a decrease in other immune cells, and tear fluid cytokines returning to initial levels.Conclusion/SignificanceOur NHP model accurately reproduces acute trachoma clinical signs, allowing for the precise assessment of the local immune responses in infected eyes. A progressing immune response occurred for weeks after exposure to Ct, which subsided into persistence of innate immune responses. Understanding these local responses is the first step towards using the model to assess new vaccine and therapeutic strategies to prevent disease.Author SummaryChlamydia trachomatisis the leading infectious cause of blindness worldwide. The pathogenesis of trachoma is more complicated than other types of bacterial conjunctivitis: clinical signs of trachoma are rooted in repeatedChlamydia trachomatisinfections of the inner eyelid surfaces, which roughens the skin. This lead to eyelid deformation and lashes rubbing on the cornea, which across multiple years of abrasion, ends with corneal opacification. The immune system is a pivotal aspect of disease, involved in disease aggravation, but also key for exploitation in development of a trachoma vaccine. Here we describe a non-human primate model of trachoma that accurately reproduces acute human eye disease, allowing for the precise assessment of the local immune responses in infected eyes. A progressing immune response occurred 4 weeks after exposure to Ct, which subsided into persistence of innate immune responses. Understanding these local responses is the first step towards using the model to assess new vaccine and therapeutic strategies to prevent disease.

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“…Studies of other eye diseases in which an immunopathological mechanism may be suspected have shown that secretory IgA levels are normal or reduced, while IgG concentrations are high in cases with corneal ulcer (10) and reduced in cases with trachoma (44,56). The concentrations of the complement factors G3 and C4 have been found to deviate in the patients with corneal ulcer and trachoma (10) compared with healthy persons (69).…”

Section: Immunoglobulins and Other Proteins In Saliva And Tear Fluidmentioning

confidence: 99%

Sjögren's Syndrome

Manthorpe

Frost‐Larsen

Isager

et al. 1981

Allergy

140

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Immunoglobulins in tear in trachoma patients.

Cited by 9 publications

References 5 publications

Localization of IgG in the normal and dystrophic rat retina after laser lesions*

Localization of IgG in the normal and dystrophic rat retina after laser lesions*

Multimodal mucosal and systemic immune characterization of a novel non-human primate trachoma model highlights the critical role of local immunity during acute phase disease

Sjögren's Syndrome

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