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Age-related macular degeneration (AMD) involves degenerative and neovascular alteration in the macular region of the retina resulting in central vision loss. AMD can be classified into dry (dAMD) and wet AMD (wAMD). There is no established treatment for dAMD, and therapies available for wAMD have limited success. Diagnosis in early AMD stages is difficult due to the absence of clinical symptoms. Currently, imaging tests are used in the diagnosis of AMD, but cannot predict the clinical course. The clinical limitations to establishing a diagnosis of AMD have led to exploration for innovative and more sensitive tests to support the diagnosis and prognosis of the disease. MicroRNAs (miRNAs) are small single-stranded non-coding RNA molecules that negatively regulate genes by post-transcriptional gene silencing. Because these molecules are dysregulated in various processes implicated in the pathogenesis of AMD, they could contribute to the early detection of the disease and monitoring of its progression. Studies of miRNA profiling have indicated several miRNAs as potential diagnostic biomarkers of AMD, but no approved biomarker is available at present for early AMD detection. Thus, understanding the function of miRNAs in AMD and their use as potential biomarkers may lead to future advances in diagnosis and treatment. Here we present a brief review of some of the miRNAs involved in regulating pathological processes associated with AMD and discuss several candidate miRNAs proposed as biomarkers or therapeutic targets for AMD.

A key aspect of the inflammatory phenomenon is the involvement of costimulatory molecules expressed by antigen-presenting cells (APCs) and their ability to secrete cytokines to set instructions for an adaptive immune response and to generate tolerance or inflammation. In a novel integrative approach, we aimed to evaluate the kinetic expression of the membrane and soluble B7 costimulatory molecules CD86, ICOS-L, PDL1, PDL2, the transcription factor Interferon Regulatory Factor 4 (IRF4), and the cytokines produced by monocyte-derived dendritic cells (Mo-DCs) after challenging them with different concentrations of stimulation with E. coli lipopolysaccharide (LPS) for different lengths of time. Our results showed that the stimuli concentration and time of exposure to an antigen are key factors in modulating the dynamic expression pattern of membrane and soluble B7 molecules and cytokines.

Introduction Allergic conjunctivitis (AC) is one of the most frequent ophthalmological diseases. AC is characterized by ocular surface inflammation and systemic immune dysregulation with low frequency of CD4+CD25+FOXP3+ regulatory T cells and higher frequency of circulating effector T cells. It has been reported that α-melanocyte stimulating hormone (α-MSH) constitutes one of the principal mechanisms of immune regulation in the anterior chamber of the eye and the ocular surface, promoting the differentiation of Tregs in a murine model of experimental autoimmune uveitis and suppressing autoreactive T cells in a murine model of experimental autoimmune encephalomyelitis. This work aimed to evaluate the involvement of α-MSH in Tregs induction in cells obtained from patients with AC. Methods Peripheral blood mononuclear cells (PBMC) were obtained from blood sampling after assent consent was obtained from pediatric patients sensitized to house dust mite (HDM) and diagnostic with AC. PBMC were cultured with HDM and/or α-MSH. After 72h of culture, PBMC were harvested and stained with anti-CD4-AmCyan, anti-CD25-PE, anti-FOXP3-FITC and anti-CD69-APC-Cy7 and analyzed by flow cytometry. IL-2, IL-4, IL-6, IL-10, IL-17, TNF-a and IFN-γ were determined by cytometric bead arrays. Results A significant increase in the frequency of CD4+CD25+FOXP3+ T cells and a significant decrease in the frequency of CD4+CD69+ cells were observed in HDM+α-MSH stimulated cells, when compared with HDM. Remarkably, IL-4 showed a significant decrease in cultured cells stimulated with HDM+α-MSH. Conclusion These results suggest that a-MSH inhibit the IL-4 production, reestablishing the development of Treg cells and control pathogenic CD4+CD69+ T cells.

Allergic conjunctivitis (AC) is an inflammation of the conjunctiva secondary to an immune response to exogenous antigens, usually called allergens. In fact, AC is a syndrome that involves the entire ocular surface, including conjunctiva, lids, cornea, and tear film. The signs and symptoms of AC have a meaningful effect on comfort and patient health, and could be influenced by environment, genetics and immune regulation mechanisms, all of which work together in a complex immunological homeostasis. Dysregulation in such immune responses could turn into a variety of ocular allergic diseases (OAD). This review describes some of the current understanding of cellular and molecular pathways involved in different OAD.La conjuntivitis alérgica es la inflamación de la conjuntiva secundaria a una respuesta inmunitaria contra antígenos exógenos, usualmente llamados alergenos. De hecho, la conjuntivitis alérgica es un síndrome que involucra la totalidad de la superficie ocular, incluyendo la conjuntiva, los párpados, la córnea y la película lagrimal. Los signos y síntomas de la conjuntivitis alérgica tienen un efecto significativo en el bienestar y salud del paciente y pueden ser influidos por el ambiente, la genética y mecanismos de regulación inmunológicos, todos los cuales trabajan en conjunto en una compleja homeostasia inmunológica. La disregulación de estos mecanismos puede desembocar en una gran variedad de enfermedades alérgicas oculares. Esta revisión describe algunos de los conocimientos celulares y moleculares actuales, involucrados en las diferentes enfermedades alérgicas oculares.

Human Limbal Epithelial Cells (hLEC) are stem cells that give rise to corneal epithelium. After corneal damage, hLEC produce large amounts of IL-8 and IL-6, inducing inflammation in cornea and conjunctiva. Despite inflammation is necessary to repair the ocular surface since this process may be potentially harmful and could lead to corneal opacity. Ophthalmic infectious diseases have been treated with human dialyzable leukocyte extracts (hDLE). Clinical observations in hDLE-treated patients, have suggested an apparent control of ocular inflammatory injuries, without changes in the re-epithelialization process.To determine the inflammatory cytokine profile in supernatants (SN) of hLEC cultured with hDLE.hLEC were obtained from cadaver donors. hDLE were added to the hLEC cultures, and SN were collected at different times (1h, 3h, 6h, and 24h). IL-1?, IL 6, IL-8, IL-12p70 and TNF-? were measured in SN with cytometric bead arrays.The majority of isolated cells were CK19+/vimentin+/p63+, indicating that cultured-cells were limbal epithelial stem cells. Limbal cells responded to hDLE by diminishing the secretion of IL-8 and IL-6. Secretion of IL-8 and IL-6 was down-regulated significantly at 24h of culture with hDLE. Interestingly, hDLE did not induce secretion of IL-1 ?, TNF-?, and IL-12p70 in hLEC at any evaluated times.hDLE down-regulates secretion of IL-8 and IL-6 without induction of IL-1 ?, TNF-a, and IL-12p70 in hLEC. Our results provide a basis to understand some clinical effects, related to control ocular inflammation, that have been observed in patients treated with hDLE.