Biomedical subjects

C C Chan

Publications and source records attributed to C C Chan.

At least 415 records · Page 23Linked to original sources

PubMed1988

Suramin keratopathy.

Vortex keratopathy occurred in six patients given high-dose intravenous suramin for adrenocortical carcinoma. The corneal findings were bilateral and symmetric. Two patients complained of foreign-body sensation. One patient developed opacities of the anterior lens epithelium. Histopathologic studies of the eyes in one patient showed intraepithelial apical deposits in the cornea, conjunctiva, and lens epithelia. By electron microscopy, these deposits were found to be membranous lamellar inclusion bodies. These findings, as demonstrated by osmium-PAS staining and electron microscopy, were similar to those in other drug-induced lipid storage diseases.

Adrenal Cortex↗

PubMed1988

Immunopathologic study of Vogt-Koyanagi-Harada syndrome.

We studied an enucleated eye from a patient with a 30-year history of Vogt-Koyanagi-Harada syndrome using both conventional and immunohistochemical techniques. Clinically, the eye was in the end stage of Vogt-Koyanagi-Harada syndrome, and was characterized by the absence of inflammation, large areas of chorioretinal scarring, and pigmentary changes. Histopathologic examination showed marked retinal gliosis, extensive chorioretinal adhesion and scar formation, migration of pigment into the retina, and severe retinal pigment epithelial changes. However, foci of mild to moderate nongranulomatous inflammation of the uvea were observed. These foci contained infiltrating cells that were mainly T lymphocytes with B lymphocyte aggregates at the center. Scattered macrophages were also noted in the uvea and retina. These findings suggest that both the cell-mediated and humoral immune arms may play roles in the pathogenesis of Vogt-Koyanagi-Harada syndrome.

Aged↗

PubMed1988

Coexpression of neuronal, glial, and major histocompatibility complex class II antigens on retinoblastoma cells.

This study identifies the presence of major histocompatibility complex class II antigens on retinoblastoma cells. In addition, the modulation of HLA-DR by interferon-gamma as well as the preferential expression of this major histocompatibility complex molecule over HLA-DQ is described. Double labeling experiments revealed that HLA-DR antigen is shared concomitantly with cells of glial and neuronal character. Investigations such as these underscore the possibility that expression of major histocompatibility complex class II antigens may function as immunological components in the host or play a role in the cellular differentiation of these tumor cells.

Antigens↗

PubMed1988

A new model of autoimmune disease. Experimental autoimmune uveoretinitis induced in mice with two different retinal antigens.

Experimental autoimmune uveoretinitis (EAU) is an organ-specific, T lymphocyte-mediated autoimmune disease, which serves as a model for several human ocular inflammations of an apparently autoimmune nature. EAU pathology in some rodents and in monkeys can readily be induced by immunization with several different retinal proteins; however, advancing research into the cellular mechanisms of this disease has raised the need for an EAU model in an immunologically and genetically well defined species. We report here the induction of EAU in the mouse, which has hitherto been considered a species refractory to EAU, with two retinal Ag, the retinal soluble Ag and the interphotoreceptor retinoid-binding protein. Although all the mouse strains tested exhibited lymphocyte responses and antibody titers to both retinal Ag, EAU was inducible in only some of the strains, and the uveitogenic responses to retinal soluble Ag and interphotoreceptor retinoid-binding protein appeared to be mutually exclusive. The EAU model in mice was found to differ in several respects from the EAU model in other rodent species. Induction of the disease was achieved with a relatively high dose of Ag and an intensified immunization protocol, and the onset of disease was later, the duration was longer, and the course was less acute. Anterior segment involvement was slight or nonexistent, and damage to the retina and uvea was of a focal rather than of a diffuse nature. Murine EAU appeared to approximate some types of human uveitis more closely than the EAU models described in other rodent species with respect to its pathologic manifestations as well as its more chronic course. The relatively longer duration of the active stage of disease in murine EAU should facilitate therapeutic intervention in established disease, which was not feasible in the more acute models of EAU. The extensive knowledge of the immunologic parameters of the mouse and the availability of genetically defined strains should be of great value in the study of cellular mechanisms and immunogenetics of ocular autoimmune disease.

Animals↗

PubMed1988

Immunohistochemical markers in the normal human epibulbar conjunctiva from fetus to adult.

Monoclonal antibodies were used for the study of inflammatory cellular subtypes, Langerhans' cells, and major histocompatibility complex class II antigens on the epibulbar conjunctiva obtained from individuals ranging in age from fetus to the seventh decade to compile basic data for comparison with other inflammatory and proliferative conjunctival diseases. In the fetal conjunctiva, there were significantly fewer T cells and Langerhans' cells than in adult conjunctiva. In the adult conjunctiva, a mild T-cell infiltration was observed. Expression of HLA-DQ in the 20- to 50-year-old age group was significantly lower compared with fetal and other age groups.

Adolescent↗

PubMed1988

Iris inflammatory cells, fibronectin, fibrinogen, and immunoglobulin in various ocular diseases.

Using immunohistochemical techniques, we analyzed the inflammatory cell subpopulation and the presence of fibronectin and immunoglobulin in iridectomy specimens from 50 patients with cataracts, glaucoma, and uveitis, and from ten normal eyes. The irises from patients with uveitis showed the highest numbers of T-lymphocytic infiltration compared with all other groups. Concentrations of fibronectin, fibrinogen, and immunoglobulins were significantly higher in the uveitic group compared with other diseases and normal controls. The irises from patients with glaucoma showed fewer infiltrating cells and less fibronectin and fibrinogen. Enhancement of major histocompatibility complex class II antigen HLA-DR expression was observed in all disease groups compared with controls. These findings suggest that in patients with uveitis and acute glaucoma the infiltrating T lymphocytes and the presence of fibronectin, fibrinogen, and immunoglobulins may contribute to the greater risk of postsurgical inflammation, leading to such problems as closure of the iridectomy. The enhancement of HLA-DR antigen expression in the iris may indicate abnormalities of iris resident cells seen in various diseases.

Aged↗

PubMed1988

Identification of a uveitopathogenic and lymphocyte proliferation site in bovine S-antigen.

S-antigen is a well-characterized retinal protein that is highly pathogenic for the induction of experimental autoimmune uveitis (EAU), a severe inflammatory disease of the eye and the pineal gland. EAU was observed following the immunization of Lewis rats with various doses (50 to 200 micrograms) of a small synthetic peptide, peptide N (22 amino acids in length), which corresponds to amino acid positions 281 to 302 in bovine S-antigen. Peptide N consistently induced an EAU that was identical to the disease caused by native S-antigen. Clinically, the disease that developed in the eye was characterized by iris and pericorneal hyperemia, followed by inflammatory exudates in the anterior chamber and vitreous. Histopathologically, a severe inflammatory response was observed that resulted in the complete destruction of the photoreceptor cell layer of the retina. In addition, animals with ocular inflammatory disease had an associated pinealitis characterized by a lymphocytic infiltration of the pineal gland. Furthermore, draining lymph node cells of rats immunized with peptide N showed strong in vitro proliferative responses toward peptide N as measured by [3H]thymidine uptake. Our results indicate that several synthetic peptides, which correspond to the amino acid sequence of bovine S-antigen, are capable of inducing an EAU and, as such, suggest that multiple uveitopathogenic sites may be present in the molecule.

Animals↗

PubMed1988

Relationship between sympathetic ophthalmia, phacoanaphylatic endophthalmitis, and Vogt-Koyanagi-Harada disease.

The more than coincidental occurrence of phacoanaphylatic endophthalmitis (PE) in sympathetic ophthalmia, and the similarity of the dissimilarity between Vogt-Koyanagi-Harada (VKH) disease and sympathetic ophthalmia have been well described both clinically and histopathologically. The etiology and pathogenesis of these three diseases are still not fully understood. Identifying and distinctive characteristics among them include the history of ocular trauma in sympathetic ophthalmia, rupture of the lens capsule in phacoanaphylatic endophthalmitis, and involvement of the skin, ear, and central nervous system in VKH disease. A T-cell-mediated immune reaction to ocular antigens seems to play a major role in sympathetic ophthalmia and VKH disease. A B-cell-related Arthus reaction to lens antigen seems to be the principle mechanism of PE. Thus, these three diseases may represent a spectrum of uveitis. At one end is the delayed-type hypersensitivity disease of sympathetic ophthalmia, whereas at the opposite end is the immune complex disease of PE, with VKH disease in the middle of this uveitic spectrum.

Adrenal Cortex Hormones↗

PubMed1988

Clinical and immunopathological studies of pars planitis in a family.

We examined a family in which two brothers with identical HLA typing have pars planitis with snowbanking. Immunopathological studies of one of their eyes showed that in the area of snowbanking over the pars plana there was mild to moderate inflammatory cell infiltration, consisting of mostly Pan T (Leu 4+) lymphocytes. The ratio of T helper/inducer to T suppressor/cytotoxic cells was approximately 10:1. Few macrophages (OKM1+) were identified. Very few B cells and no NK cells were observed. Some retinal vessels had a perivascular infiltration consisting of mostly T lymphocytes. Most of the inflammatory cells bore class II antigens (HLA-DR+), while T cells bore few IL-2 receptors (anti-TAC+). The snowbank consisted mainly of glial elements (GFAP+) and basement membrane components (type IV collagen and laminin) with the predominant cell the Müller cell (Mü+). A site of inflammation at the iris-ciliary body junction also stained for B cells (Leu 14+). These findings suggest that the snowbank could be formed by the glial elements of the peripheral retina. The chronic inflammation in pars planitis appears to consist of helper T cells, both in the pars plana, and the retinal vasculature.

Adolescent↗

PubMed1988

Anti-Ia antibody diminishes ocular inflammation in experimental autoimmune uveitis.

An experimental model of inflammatory eye disease, experimental autoimmune uveitis (EAU), was established by injecting rats in the footpad with S-antigen in complete Freund's adjuvant. This model system was used to evaluate the role of major histocompatibility complex (MHC) class II antigens (Ia) in the pathogenesis of this T cell mediated disease. One day prior to S-antigen priming, rats were injected with either anti-Ia antibodies or with mouse ascites. Clinical and histopathological analysis of eyes from rats treated with anti-Ia antibody showed less ocular inflammation as well as a delay in onset of EAU when compared to controls (p = 0.01). Furthermore, immunocytochemical evaluation demonstrated that tissue obtained from animals receiving anti-Ia therapy also expressed less Ia antigen, as well as a diminution in the number of infiltrating macrophages and lymphocytes. These data show that anti-Ia treatment significantly modifies the course of EAU in the rat. In addition, this study suggests that MHC class II antigen expression may be involved in the initiation and continuation of immune responses that results in ocular inflammatory diseases.

Animals↗

PubMed1988

Identification of the lymphokines, interferon-gamma and interleukin-2, in inflammatory eye diseases.

The exact pathogenic mechanisms involved in autoimmune and inflammatory eye diseases are not known. However, studies during the past few years indicate that a T cell infiltrate, T cell sensitization to retinal antigens and expression of major histocompatibility complex (MHC) class II antigens are associated with this process. In this report we show that the lymphokines, IL-2 and IFN-gamma, are present in the human eye during inflammatory and autoimmune diseases. The presence of these lymphokines is associated with a lymphocyte infiltrate, predominantly of T cell origin, and with the expression of MHC class II antigens on both the infiltrating cells and ocular resident cells, that is, retinal pigment epithelial (rpe) cells and retinal vascular endothelial cells. Furthermore, in vitro studies demonstrate that IFN-gamma can enhance the expression of the HLA-DR determinant on both of these cell types. These observations suggest that lymphokine induced class II antigen expression may serve as a local amplification system in autoimmune and inflammatory eye diseases. A better understanding of the role of lymphokines in the mechanisms involved in the development of autoimmunity and inflammation may be beneficial in the treatment of these diseases.

Adult↗

PubMed1988

Dynamics of experimental autoimmune uveoretinitis induced by adoptive transfer of S-antigen-specific T cell line.

Long-term S-antigen (S-Ag) specific T lymphocyte lines can induce experimental autoimmune uveoretinitis (EAU) when transferred into naive rats systemically or intravitreally. The uveitogenic lymphocyte line (ThS) stains positively for the ART 18 (IL-2 receptor) and W3/25 (T helper/inducer); negatively for OX6 (RT1B) and OX8 (T suppressor/cytotoxic cells). The inflammation induced by systemic or intravitreal transfer of the ThS line was studied with respect to the surface markers of the infiltrating cells, as well as the markers expressed by the resident ocular cells, by immunohistopathological techniques. On day 4 to 5 after systemic injection of the ThS line, rare T cells (W3/25+, ART 18+) and macrophages (OX42+, OX6+) surrounded by some resident cells that expressed MHC class II antigens were identified in the ciliary body and choroid. Shortly thereafter (10-20 hr) more macrophages, polymorphonuclear leukocytes, and T lymphocytes (W3/25+, then OX8+) appeared in the inflamed eye. The kinetics was similar to EAU induced by active immunization. The rats with severe disease expressed the MHC class II antigens on large numbers of resident cells in the eye. Intravitreally transferred ThS cells migrated to the retina within 24 hr of transfer. Infiltration of macrophages (OX6+, OX42+) and other T lymphocytes (OX6+, W3/25+ or OX8+), in conjunction with photoreceptor damage, were observed within the next 24-48 hr. The cells with the ThS markers disappeared from the eye on day 4-5 post transfer. These findings suggest that the ThS line can recognize the photoreceptor S-Ag in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Iris lymphocytic infiltration in patients with clinically quiescent uveitis.

Iridectomy specimens from 16 patients with clinically quiet chronic uveitis were analyzed by immunoperoxidase staining and compared to control iridectomy specimens from 11 non-uveitic patients. Nine of 16 uveitis specimens and none of the control specimens demonstrated a lymphocytic infiltrate consisting of interleukin-2 receptor-negative T helper and suppressor cells (P less than .003). Class II antigens were detected in the iris stroma in all uveitis specimens and six of the controls (P less than .006). Despite a quiescent clinical state, patients with chronic uveitis have increased expression of class II antigens in uveal tissue and have significant uveal infiltration of T helper and suppressor cells. These findings in a variety of types of uveitis give additional support for the importance of delayed type hypersensitivity mechanisms in human uveitic disease.

Adolescent↗

PubMed1987

Histopathologic and immunohistopathologic features of subretinal fibrosis and uveitis syndrome.

We studied histopathologic and immunohistopathologic features of an eye from a patient who had hypopigmented choroidal lesions with subsequent development of progressive subretinal fibrotic tissue associated with minimal signs of vitreal inflammation. A 24-year-old woman had a rapid and severe onset of the disease, which led to blindness within a few months despite treatment with corticosteroids and cyclophosphamide. Histopathologic studies disclosed a marked gliotic retina and thick subretinal fibrotic tissue as well as a granulomatous lymphocytic infiltration in the choroid. Electron microscopy demonstrated that the subretinal tissue was derived from retinal pigment epithelial cells. The immunoperoxidase staining showed similar proportions of T and B lymphocytes, indicating a relative increase of B cells. There was a predominance of the helper/inducer T lymphocyte subset in the infiltrating area. The Müller cells in the retina expressed class II antigens of the major histocompatibility complex.

Adult↗

PubMed1987

Effects of two novel inhibitors of 5-lipoxygenase, L-651,392 and L-651,896, in a guinea-pig model of epidermal hyperproliferation.

The effects of two novel and structurally different 5-lipoxygenase inhibitors, L-651,392 (4-bromo-2,7-dimethoxy-3H-phenothiazin-3-one) and L-651,896 (2,3-dihydro-6-(3-(2-hydroxymethyl)phenyl-2-propenyl)-5-benzo furanol), on epidermal proliferation were examined in the guinea-pig ear stimulated with the calcium ionophore A23187. Topical application of A23187 on the guinea-pig ear induced epidermal hyperproliferation which could be quantitated by tritiated-thymidine incorporation into DNA in the heat-separated epidermis. The ionophore-induced response was inhibited dose dependently by either L-651,392 or L-651,896 when the guinea-pigs were pretreated topically with these compounds. In separate experiments, it was demonstrated that A23187 induced a significant increase in the levels of immunoreactive-LTB4 in the guinea-pig ear which could be blocked by either inhibitors. It was suggested that L-651,392 and L-651,896 inhibited the ionophore-induced epidermal proliferation via their inhibitory action on the 5-lipoxygenase pathway of arachidonic acid metabolism.

Animals↗

PubMed1987

Immunopathology and electron microscopy of Acanthamoeba keratitis.

In order to evaluate the local cellular immune response to Acanthamoeba infection we performed immunohistochemical examinations of the corneal buttons of two patients with Acanthamoeba keratitis. We found that the corneal stroma was infiltrated with polymorphonuclear leukocytes and HLA-DR positive macrophages that appeared to be stromal keratocytes by light microscopy. Despite the presence of chronic inflammation in both patients, no stromal lymphocytes were seen in one patient and a sparse lymphocytic infiltrate was seen in the other patient. Electron microscopy confirmed the presence of macrophages, neutrophils, and Acanthamoeba organisms in these two patients.

Adult↗

PubMed1987

Retinal vascular endothelium expresses fibronectin and class II histocompatibility complex antigens in experimental autoimmune uveitis.

To analyze the role of the retinal vascular endothelial cells in the development of experimental autoimmune uveitis (EAU), we studied the presence of Ia antigen and FN in retinal vessels of Lewis rats immunized with retinal S antigen. Immunopathologic studies were performed on frozen tissues obtained during various stages of the disease. Our results show that Ia antigen was not present in the normal rat retina, and there was very little FN present in a few retinal vessels. One to two days prior to the histologic and clinical onset of EAU, FN was found to be increased in the retinal vessels. Ia antigen was found to be present in the retinal vessels coincident with the first signs of cellular infiltration. During the stage of maximal cellular infiltration, FN was present diffusely throughout the retina, as well as in the subretinal space, and Ia antigen was found diffusely in the cellular infiltrate. Therefore, FN and Ia antigen reflect the immunomodulation of vascular endothelial cells in EAU, which may be very important in the pathogenesis of retinal S antigen-induced uveitis. Two possible mechanisms for the role of the activation of the retinal vascular endothelium in the development of retinal inflammation in uveitis are discussed.

Animals↗

PubMed1987

Immunohistopathology of ocular sarcoidosis. Report of a case and discussion of immunopathogenesis.

An eye from a patient with systemic sarcoidosis and active ocular involvement was studied by the use of monoclonal antibodies and the immunoperoxidase technique to identify the subtypes of infiltrating cells and the presence of lymphokines. Large numbers of lymphoid cells reacting with anti-pan T cell (Leu-4) and anti-T helper/inducer (Leu-3a) subsets were observed around and within sarcoid granulomas. Only rare T suppressor/cytotoxic cells (Leu-2a) were observed. B lymphocytes and plasma cells were present in a few foci. Within the granuloma, T lymphocytes, macrophages, and epithelioid cells showed membrane labeling for interleukin 2 receptors and interferon gamma. We demonstrate the in vivo expression of interleukin 2 receptors and the release of interferon gamma by mononuclear phagocytes and T lymphocytes in ocular sarcoidosis, and we theorize about the activated T helper cell-derived lymphokines in macrophage activation and sarcoid granuloma formation in the eye.

Adult↗