Cellular immune response of patients with uveitis to peptide M, a retinal S-antigen fragment

Nityanand, Soniya; Singh, Vijay K.; Shinohara, Toshimichi; Paul, Abhirup; Agarwal, Paresh; Agarwal, S. S.

doi:10.1007/bf00920244

Cited by 11 publications

(3 citation statements)

References 31 publications

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“…Intermediate uveitis has also been associated with the HLA-DR15 haplotype (49,50). T-cell responses to the immunodominant epitope of retinal arrestin, peptide M, have been documented in several populations of uveitis patients (51)(52)(53). The immunodominant T-cell epitope of MBP has been localized to residues 82-98; this MBP peptide binds with high affinity to the disease-associated HLA-DR2 molecule, and is recognized by HLA-DR2-restricted T-cell clones from MS patients (54).…”

Section: Discussionmentioning

confidence: 99%

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

et al. 2007

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Introduction-Although myelin autoimmunity is known to be a major factor in the pathogenesis of multiple sclerosis (MS), the role of nonmyelin antigens is less clear. Given the complexity of this disease, it is possible that autoimmunity against nonmyelin antigens also has a pathogenic role. Autoantibodies against enolase and arrestin have previously been reported in MS patients. The Tcell response to these antigens, however, has not been established.

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Section: Discussionmentioning

confidence: 99%

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

et al. 2007

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“…It can be induced by many autoantigens of intraocular cells. Animal models have identified retinal S-antigen/arrestin (S-Ag) ( Caspi, 2011 ), interphotoreceptor retinoid-binding protein (IRBP) ( Bieganowska et al, 1997 ), rhodopsin ( de Smet et al, 1990 ), opsin ( Yamamoto et al, 1993 ), phosducin ( Gery et al, 1994 ), recoverin ( Dua et al, 1992 ), Rpe65 ( Nityanand et al, 1993 ), melanin ( Nakamura et al, 2005 ), and lens proteins and cellular retinaldehyde-binding protein ( Broekhuyse et al, 1993 ) as “uveitogenic”. Now, EAU is generally used as experimental models of uveitis to study the immunopathologic mechanisms of human intraocular inflammatory diseases.…”

Section: Key Role Of Tumor Necrosis Factor-alpha In Understanding Uveitismentioning

confidence: 99%

TNF-α in Uveitis: From Bench to Clinic

Jiang

Tao

et al. 2021

Front. Pharmacol.

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Uveitis is an inflammation of the iris, ciliary body, vitreous, retina, or choroid, which has been shown to be the first manifestation of numerous systemic diseases. Studies about the immunopathogenesis and treatment of uveitis are helpful to comprehend systemic autoimmune diseases, and delay the progression of systemic autoimmune diseases, respectively. Tumor necrosis factor-alpha (TNF-α), a pleiotropic cytokine, plays a pivotal role in intraocular inflammation based on experimental and clinical data. Evidence of the feasibility of using anti-TNF-α agents for uveitis management has increased. Although there are numerous studies on TNF-α in various autoimmune diseases, the pathological mechanism and research progress of TNF-α in uveitis have not been reviewed. Therefore, the objective of this review is to provide a background on the role of TNF-α in the immunopathogenesis of uveitis, as well as from bench to clinical research progress, to better guide TNF-α-based therapeutics for uveitis.

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“…Norway) as described elsewhere [18]. After three washings cells were adjusted to 1 x 106 cells/ml in complete media.…”

Section: La K Cell Assaymentioning

confidence: 99%

Effect of Elevated Temperature on Cytotoxic Effector Cells

Singh¹,

Biswas²,

Pandey

et al. 1996

Pathobiology

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Several studies have shown a direct correlation between temperature and immune response. The effect of elevated temperature on cytotoxic effector functions is not well known. In the present study we have investigated the effect of elevated temperatures (38.5 and 40 °C) on cytotoxicity of lymphokine-activated killer cells (LAK), monocyte cytotoxicity, cytotoxic T lymphocytes (CTL) and tumor necrosis factor (TNF)-mediated cytotoxicity, and compared them with results at 37°C. LAK cell cytotoxicity was inhibited significantly at 40°C (p < 0.01) and there was no marked difference at 38.5°C (p = 0.17) as compared to 37 °C when natural killer (NK)-sensitive K562 cells were used as target. When NK-resistant Raji cells were used as a target, cytotoxicity was inhibited at 40°C (p = 0.33). Monocyte cytotoxicity was enhanced at 40°C (p= 0.19) as well as at 38.5°C (p = 0.38) as compared to 37°C but differences were not statistically significant. Lipopolysaccharide (LPS) enhanced monocyte cytotoxicity. LPS-stimulated enhancement was further enhanced significantly at 40°C (p < 0.05) and 38.5°C (p < 0.05). Cytotoxicity of CTL was significantly inhibited at 38.5 compared to 37°C (p < 0.0002). TNF-mediated cytotoxicity was significantly enhanced at 40°C (p < 0.0004) and 38.5°C(p < 0.001).

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Cellular immune response of patients with uveitis to peptide M, a retinal S-antigen fragment

Cited by 11 publications

References 31 publications

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

TNF-α in Uveitis: From Bench to Clinic

Effect of Elevated Temperature on Cytotoxic Effector Cells

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