Biomedical subjects

W R Green

Publications and source records attributed to W R Green.

At least 91 records · Page 5Linked to original sources

PubMed1997

Histologic study of a shielded macula.

PURPOSE: To illustrate the histologic changes at the macula of an eye shielded from focused light for 76 years. Age-related macular degeneration with a central, subretinal, fibrous scar was present in the fellow eye. METHODS: Autopsy examination of both eyes of a 91-year-old man was performed. The superior half of the macular area of the shielded eye was studied by light microscopy, and the inferior half was studied by electron microscopy. Serial sections through the macular area of the fellow eye were prepared and studied. RESULTS: The shielded eye contained basal laminar deposits up to 6.0 microns in thickness and basal linear deposits up to 1.0 micron in thickness in the macular area. The photoreceptor outer and inner segments of the outer nuclear layer were intact. The macular area of the fellow eye contained a two-component, vascularized, disciform scar that measured up to 250 microns in one area, with retinal pigment epithelial tears at the nasal and temporal margins. Extensive photoreceptor layer atrophy was present. CONCLUSIONS: Such marked asymmetry of macular degeneration in this case may be further evidence of the role of light exposure in the development of age related macular degeneration.

Aged↗

PubMed1997

Ophthalmomyiasis interna posterior. Report of a case with optic atrophy.

PURPOSE: The prognosis for patients with ophthalmomyiasis Interna posterior is variable. In many patients the larva remains in the eye for years without inducing inflammation or loss of vision. Sometimes, however, the migrating larva involves the macula and optic nerve and results in permanent visual loss or even blindness. METHODS: Our patient presented with sudden painless loss of vision in the right eye that was caused by ophthalmomyiasis interna posterior. Hemorrhage of the optic nerve head suggested that the fly larva had entered the vitreous cavity from the optic nerve head. Subretinal tracts were sequelae of the subretinal migration of the organism. Sequential photographs documented the fly larva migration into the optic nerve head head from the vitreous cavity. The organism was removed by pars plana vitrectomy and retinectomy. RESULTS: In spite of the successful removal of the first stage fly larva, the visual acuity remained poor because of optic nerve atrophy. CONCLUSION: We suggest early removal of fly larvae to prevent damage and visual loss in cases of ocular myiasis interna posterior.

Blindness↗

PubMed1997

Clinicopathologic correlation of chorioretinitis sclopetaria.

PURPOSE: To report the clinicopathologic features in the eye of a patient who sustained a traumatic chorioretinal rupture from a gunshot wound to the orbit, chorioretinitis sclopetaria, with clinical follow up of more than 20 years. METHODS: The patient was studied ophthalmoscopically and by fluorescein angiography after the trauma and was seen intermittently thereafter. The eyes were obtained postmortem; sections of the central portion of the right eye, including the macula and optic nerve head, and the inferior cap were examined by light microscopy. RESULTS: Histopathologic study of the right eye showed partial loss of the nerve fiber and ganglion cell layers in the macular area, temporal peripapillary and macular loss of the photoreceptors with hypertrophy and hyperplasia of the retinal pigment epithelium, an epiretinal membrane, and three defects in Bruch's membrane. Inferiorly, there was a 5-mm defect in choroid, Bruch's membrane, and retina. These structures were replaced by a loose and dense fibrous connective tissue. The sclera and a long posterior ciliary nerve remained intact. A thin fibrovascular tissue from the choroid extended into the subretinal space where it was covered by retinal pigment epithelium and thickened basement membrane in the posterior aspect of the inferior lesion. Marked hemiatrophy of the optic nerve was present. CONCLUSIONS: The clinicopathologic features of chorioretinitis sclopetaria include direct traumatic chorioretinal rupture followed by marked fibrovascular proliferation with variable replacement of choroid and retina with no retinal detachment. Posteriorly, indirect macular choroidal ruptures with hyperplasia and migration of the retinal pigment epithelium into the retina and choroid, epiretinal membrane formation, loss of photoreceptors, and marked hemiatrophy of the optic nerve were present.

Adult↗

PubMed1997

An unusual case of elastofibroma oculi.

A 22-year-old female college student from the southwestern United States was first seen with progressive fluffy white growths over both corneas nasally and a history of chronic allergies and extensive sun, wind, and chlorine exposure as a competitive swimmer. The lesions were superficial, elevated, crescent-shaped, vascularized, and extended from the limbal conjunctiva onto the peripheral cornea nasally. The lesions were composed of an unencapsulated thick fibrovascular pannus with numerous fibrocytes, chronic inflammatory cells and mast cells, and abundant linear and wavy elastinophilic profiles, but no adipose tissue. Ultrastructurally, the elastinophilic structures were immature elastic fibers arranged in globules and bundles within a thick collagenous matrix. No mature elastic fibers were found. A few areas of elastotic degeneration were also found. This lesion resembled elastofibromas that have been reported more commonly in the subcapsular region and only once in the ocular region. Previous reports debated whether the elastic material in elastofibromas is derived from excessive production of elastic fibers by activated fibrocytes or from elastotic degeneration of collagen. In our case, both processes occur and are presumed to result from excessive ultraviolet radiation, wind and chlorine exposure, and perhaps, chronic inflammation; features that have been ascribed to the pathogenesis of pingueculae and pterygia.

Adult↗

PubMed1997

Upregulation of vascular endothelial growth factor in ischemic and non-ischemic human and experimental retinal disease.

Vascular endothelial growth factor (VEGF) is induced by hypoxia and it has been implicated in the development of iris and retinal neovascularization (NV) in ischemic retinopathies in which it has been suggested that Muller cells are responsible for increased VEGF production. VEGF, however, is also known to be a potent mediator of vascular permeability in other tissues and may perform this function in retina. Immunohistochemical staining for VEGF was performed on a variety of human and experimental ischemic and non-ischemic ocular disorders in which blood retinal barrier (BRB) breakdown is known to occur to determine if there is an upregulation of VEGF in these conditions. We found increased VEGF immunoreactivity in ganglion cells of rats with oxygen-induced ischemic retinopathy and in ganglion cells, the inner plexiform layer, and some cells in the inner nuclear layer of rats with experimental autoimmune uveoretinitis (EAU), in which there was no identifiable ischemia or NV. In rats with EAU, VEGF staining intensity increased from 8 to 11 days after immunization, coincident with BRB failure. These results were confirmed using two distinct anti-VEGF antibodies and by immunoblot and the immunohistochemical staining was eliminated by pre-incubating the antibodies with VEGF peptide. VEGF staining was also increased in the retina and iris of patients with ischemic retinopathies, such as diabetic retinopathy and retinal vascular occlusive disease, and in patients with disorders in which retinal ischemia does not play a major role, such as aphakic/ pseudophakic cystoid macular edema, retinoblastoma, ocular inflammatory disease or infection, and choroidal melanoma. VEGF was primarily localized within retinal neurons and retinal pigmented epithelial cells in these cases. In addition or in association with its role of inducing NV, VEGF may contribute to BRB breakdown in a variety of ocular disorders and blockage of VEGF signaling may help to reduce some types of macular edema.

Animals↗

PubMed1997

Extrusion of abnormal endothelium into the posterior corneal stroma in a patient with posterior polymorphous dystrophy.

PURPOSE: To report the presence of abnormal endothelium that extruded into the posterior corneal stroma in a patient with posterior polymorphous dystrophy. METHODS: The corneal button of a man who underwent penetrating keratoplasty for posterior polymorphous dystrophy was examined by light and electron microscopy. Immunoperoxidase staining for cytokeratins, vimentin, and the endothelial antigen recognized by monoclonal antibody 2B4.14.1 antigen was performed. Two-color immunofluorescence staining for simultaneous detection of cytokeratins and 2B4.14.1 antigen was also done. RESULTS: Much of the endothelium had characteristic features of epithelium-like cells, and abnormalities in Descemet's membrane were present. Curious oval and slit-like spaces in the posterior stroma were lined by epithelium-like endothelial cells and were continuous with the anterior chamber through defects in Descemet's membrane. CONCLUSION: These abnormalities in the posterior stroma have not previously been described in histopathologic reports of posterior polymorphous corneal dystrophy and are likely an unusual variation in the spectrum of this hereditary disorder.

Adolescent↗

PubMed1997

Endothelial metaplasia in the iridocorneal endothelial syndrome.

PURPOSE: To test the hypothesis that the aberrant, cytokeratin-expressing cells that replace endothelium in the iridocorneal endothelial (ICE) syndrome are of endothelial origin. METHODS: Corneas from four patients with Chandler's syndrome and three with essential iris atrophy were examined by two-color immunofluorescence for simultaneous expression of cytokeratins and two markers of endothelial lineage: vimentin and the antigen recognized by the antiendothelial monoclonal antibody 2B4.14.1. RESULTS: In six corneas, unequivocal endothelial staining for cytokeratins was present; in each of these, cells coexpressing cytokeratins and the two endothelial markers were clearly identifiable. In the remaining cornea, weak cytokeratin staining that colocalized with vimentin was present. CONCLUSIONS: These results lend strong support to the hypothesis that the "epithelial-like" endothelial cells in ICE syndrome are cells of endothelial lineage rather than heterotopia of epithelial cells; these cells probably arise via a metaplastic transformation of preexisting endothelium.

Adult↗

PubMed1996

Clinicopathologic correlation of submacular membranectomy with retention of good vision in a patient with age-related macular degeneration.

We present the clinicopathologic features of the eye of a patient with age-related macular degeneration who underwent submacular membranectomy and had retention of good visual acuity for almost 4 years despite recurrent choroidal neovascularization treated with krypton laser photocoagulation and mild expansion of the laser lesion with time. Histopathologic study of the surgically removed membrane from the right eye disclosed a thin fibrovascular membrane lined by retinal pigment epithelium on one surface. Microscopic examination of the right eye obtained post mortem disclosed a 2.75-mm (horizontal) x 2.1-mm (vertical) retinal pigment epithelium defect with overlying photoreceptor cell atrophy centered on the temporal parafoveal area, and a 0.6 x 0.1-mm subretinal pigment epithelium fibrovascular membrane with an area of retinal pigment epithelial hyperplasia and vascularization from the retina 0.4 mm temporal to the fovea. Basal laminar deposit was present in the region of the fovea and nasal parafoveal area.

Aged↗

PubMed1996

Blood-aqueous barrier in pseudoexfoliation syndrome: evaluation by immunohistochemical staining of endogenous albumin.

BACKGROUND: Alterations of the integrity of the blood-aqueous barrier (BAB) are frequent findings in eyes with pseudoexfoliation syndrome (PSX). METHODS: Immunohistochemical staining for the demonstration of albumin was used to analyze the BAB in 10 eyes with PSX without previous intraocular surgery and in 10 age-matched normal control eyes. RESULTS: In eyes with PSX, small amounts of albumin were detected along the anterior surface of the iris in 7, in the anterior chamber in 1, along the ciliary epithelium in 4, and in the trabecular meshwork in 9 of 10 eyes. PSX material was also immunoreactive. In the 10 normal control eyes, albumin was detected anterior to the iris stroma in 1 eye, in the anterior chamber in 2 eyes, in the trabecular meshwork in 1 eye, but not internal to the ciliary epithelium. CONCLUSIONS: Our findings indicate that impairment of the BAB in PSX can be localized at the level of the iris and, less frequently or to a lesser extent, at the level of the ciliary body.

Aged↗

PubMed1996

In vivo effects of locally secreted IL-10 on the murine antitumor immune response.

BACKGROUND: Interleukin-10 (IL-10) is a cytokine secreted by the TH2 class of murine lymphocytes that suppresses the secretion of interferon-gamma (IFN-gamma) by TH1 lymphocytes and inhibits macrophage-mediated T-cell stimulation and cytotoxicity. The observation that IL-10 is produced by human carcinomas in vitro and in vivo led to the hypothesis that this cytokine plays a role in the suppression of the human anti-tumor immune response. We tested this hypothesis in a murine model. METHODS: To evaluate the effect of IL-10 on the induction of an anti-tumor immune response, mice were immunized with tumor cells transfected with the IL-10 gene and then challenged with parental tumor. The effect of the local secretion of IL-10 on an established immune response was tested by immunizing mice with parental tumor and then challenging with IL-10-secreting tumors. RESULTS: IL-10-secreting tumors were as effective immunogens as control tumors. Immune mice rejected IL-10-secreting tumors as readily as control challenge tumors. In an in vitro assay, IL-10 did not inhibit CD8 lymphocyte secretion of IFN-gamma in response to tumor stimulation. One IL-10-secreting tumor clone regressed when injected into naive mice and induced an antigen-specific immune response capable of protecting mice from subsequent tumor challenge. CONCLUSIONS: The local secretion of IL-10 did not inhibit either the induction of an antitumor immune response or the ability of established effector cells to reject challenge tumors. In contrast to its effect on TH1 lymphocytes, IL-10 does not inhibit IFN-gamma secretion by CD8 lymphocytes.

Animals↗

PubMed1996

Clinicopathologic correlation of an untreated macular hole and a macular hole treated by vitrectomy, transforming growth factor-beta 2, and gas tamponade.

PURPOSE: To study the clinicopathologic features of an untreated macular hole in the right eye and a macular hole in the left eye treated by vitrectomy, application of transforming growth factor-beta 2, and gas tamponade. METHODS: The patient, a 73-year-old man with bilateral macular holes, was studied clinically before and after surgical treatment of the macular hole in his left eye. The patient's eyes were obtained postmortem and serially step-sectioned through the macula and optic nerve head for electron microscopy. RESULTS: Examination of 1-micron thick plastic-embedded sections through the macula of the right eye disclosed a 0.6-mm macular hole with rounded gliotic margins, a thin epiretinal membrane, and parafoveal cystic changes. Examination of 1-micron thick plastic-embedded sections through the macula of the left eye disclosed a 0.25-mm defect in the fovea, which was bridged by glial cells. The glial cells were continuous with a thin hypocellular epiretinal membrane without contraction features on both sides of the defect. The ultrastructural features of the glial cells were consistent with Mueller cells. CONCLUSIONS: Treatment of a macular hole with vitrectomy, transforming growth factor-beta 2, and gas tamponade was followed by complete closure of the macular hole by Mueller cell proliferation.

Aged↗

PubMed1996

[Combined true exfoliation and pseudoexfoliation of the anterior lens capsule].

BACKGROUND: True exfoliation of the lens capsule is rare, and its occurrence with pseudoexfoliation in the same eye is very unusual. CASE REPORT: An 81-year-old female presented with bilateral cataracts and a history of working with ceramics in her home kiln. Slit-lamp examination revealed pseudoexfoliation. She underwent intracapsular cataract extraction and sector iridectomy in both eyes. Light and electron microscopy of the lenses revealed a central area of splitting of the anterior lens capsule into a thin anterior and a thicker posterior layer, and deposits pseudoexfoliation material on the anterior lens capsule, on the iris pigment epithelium, and in the iris stroma. CONCLUSIONS: We interpret our findings as representing a combination of true exfoliation and pseudoexfoliation, but we did not observe any signs that might indicate a correlation or a common pathogenesis of the two conditions. Although they may occur in one eye, true exfoliation of the lens capsule and pseudoexfoliation are two unrelated distinct entities.

Aged↗

PubMed1996

Impaired generation of anti-AKR/Gross murine leukemia virus cytotoxic T lymphocytes in mice experimentally infected with MuLV.

C57BL/6 (B6) and C57BL/6.Fv-1n (B6.Fv-1n) mice mount AKR/Gross murine leukemia virus (MuLV)-specific cytolytic T lymphocyte (CTL) responses following primary and secondary stimulation with AKR/Gross MuLV-induced tumor cells. In contrast, mice exposed to infectious virus rather than virus-infected cells generate little, if any, antiviral CTL activity. In this report, we show that inoculation of B6 or B6.Fv-1n mice with MuLV prior to priming with H-2-matched AKR/Gross virus antigen-positive tumor cells resulted in a profound inhibition of the virus-specific CTL response. Antiallogeneic major and minor histocompatibility antigen-specific CTL responses were not significantly diminished in MuLV-infected mice. The AKR/Gross MuLV-specific CTL response in B6 mice was inhibited by NB-tropic (SL3-3NB, Friend and Moloney), but not N-tropic (AKR623) MuLV, suggesting that productive infection of host cells was required. We were unable to inhibit the in vitro generation of virus-specific CTL by adding modulator cells from virus-infected mice to mixed lymphocyte-tumor cell cultures (MLTC) of spleen cells from uninfected animals. We also failed to augment CTL generation in MLTC from virus-infected animals by adding exogenous IL-2 or CD4+ lymphocytes from uninfected, tumor-primed mice. Taken together, the data suggested that the inhibition resulted from either a direct or an indirect effect on the in vivo priming of virus-specific CD8+ cells. It is therefore interesting that MuLV such as Friend and Moloney, which do not encode the immunodominant epitope recognized by anti-AKR/Gross MuLV CTL, are nonetheless able to specifically inhibit this response. These results demonstrate a potentially important mechanism by which retroviruses may escape CTL-mediated immunity.

3T3 Cells↗

PubMed1996

Intrastromal epithelial accretion follows deep excimer annular keratectomy.

The purpose of this study was to evaluate corneal reepithelialization and wound healing following annular excimer keratectomy. Two sets of experiments were performed on 35 rabbit eyes. In the first set of experiments, experiment I, deep Fresnel excimer keratectomy was performed, with a 6-mm outer and 3-mm inner diameter. Animals were sacrificed at 1, 5, 12, and 16 weeks, and corneas were examined by light and electron microscopy. In experiment II, the central epithelium was left intact, and superficial and deep mid-peripheral excimer annular keratectomies were performed measuring 6 mm in outer and 3 mm in inner diameter. Animals were sacrificed at 1 week, and corneas were examined by light microscopy. Following deep Fresnel excimer keratectomy (experiment I), corneas showed stromal edema in the central 3-mm zone. Intrastromal islands of epithelial cells with PAS positive basement membrane-like structures were seen histologically at 1 week. Electron microscopy showed loss of stromal collagen in areas adjacent to epithelial islands; in areas distant from the epithelial islands, the stromal collagen appeared normal. The overlying central stroma sloughed after 5 weeks. Anterior stromal scarring was observed. In experiment II (mid-peripheral annular keratectomy), intrastromal epithelial accretion was present in corneas with deep annular keratectomy but not in superficial annular keratectomy. Intrastromal epithelial accretion follows deep excimer annular keratectomy and is associated with adjacent stromal degradation.

Animals↗

PubMed1996

Tumor detachments of the retinal pigment epithelium in ocular/ central nervous system lymphoma.

BACKGROUND: Ocular/central nervous system (CNS) lymphoma is a B-lymphocyte-derived tumor that characteristically involves the retina, optic nerve head, vitreous, and subretinal pigment epithelial areas of the eye. METHOD: A retrospective analysis of clinical history and photography fluorescein angiography, histopathology, and immunocytochemistry of an untreated patient with ocular/CNS lymphoma was performed. RESULTS: Tumor detachments of the retinal pigment epithelium (RPE) evolved into areas of RPE atrophy and depigmentation and disciform scars. Histopathologic studies disclosed foci of tumor cells in the wall of and around blood vessels and between the RPE and Bruch's membrane. Immunocytochemistry identified the malignant cells as B-lymphocytes. CONCLUSIONS: The clinicopathologic features of a patient with ocular/CNS B-cell lymphoma are presented. Retinal pigment epithelium tumor detachments evolved to areas of RPE atrophy and depigmentation and disciform scars.

Aged↗

PubMed1996

Clinicopathologic correlation of argon laser photocoagulation of retinal angiomas in a patient with von Hippel-Lindau disease followed for more than 20 years.

PURPOSE: The authors review the histopathologic findings in the eyes of a patient with multiple retinal angiomas and von Hippel-Lindau disease, who underwent treatment with argon laser photocoagulation with follow-up of more than 20 years. METHODS: The patient was studied ophthalmoscopically and by fluorescein angiography before and after argon laser photocoagulation of retinal angiomas. The eyes were obtained postmortem, and the central portion of the right eye, including the macula and optic nerve head, was sectioned serially for light microscopy. The pupil-optic nerve segment of the left eye was step-sectioned serially for light microscopy. RESULTS: Histopathologic study of the right eye disclosed mild cystoid macular edema and focal areas of exudation in the midperiphery possibly secondary to irradiation of the head. A 1.5 x 0.3-mm area of residual angioma was present in the nasal peripapillary retina. Superotemporally, four chorioretinal scars were present in one photocoagulated area. These scars were composed of dense fibrous tissue with vascularization and variable retinal pigment epithelium hyperplasia. Large, nonangiomatous vessels within each of the scars were continuous with other retinal vessels. Inferotemporally, two chorioretinal scars were present in one photocoagulated area. Histopathologically, these scars were similar to the superotemporal scars, except that no patent retinal vessels traversed the inferotemporal scars. Neovascularization of the retina was associated with one superotemporal and one inferotemporal scar. No residual angiomatous tissue was present in the supero- or inferotemporal areas. Histopathologic examination of the left eye disclosed extensive vitreous organization and periretinal fibrovascular proliferation, extensive gliosis of the retina, and a 4.5 x 2-mm schisis cavity filled with fibrinous exudate. Three angiomas with variable fibrosis were present in the left eye. CONCLUSION: Despite a poor clinical course in one eye treated with xenon arc photocoagulation, trans-scleral diathermy, and argon laser photocoagulation, a patient with von Hippel-Lindau disease and multiple retinal angiomas retained good vision in the other eye after successful treatment with argon laser photocoagulation with follow-up of more than 20 years. The amount of regression of angiomatous tissue after photocoagulation varied from lesion to lesion (complete in some; minimal in others). The authors conclude that argon laser photocoagulation of early lesions is effective in ablating smaller ( < or = 3-disc diameter) retinal angiomas.

Argon↗

PubMed1996

AKR.H-2b lymphocytes inhibit the secondary in vitro cytotoxic T-lymphocyte response of primed responder cells to AKR/Gross murine leukemia virus-induced tumor cell stimulation.

We have previously shown that AKR.H-2b congenic mice, though carrying the responder H-2b major histocompatibility complex haplotype, are unable to generate secondary cytolytic T-lymphocyte (CTL) responses specific for AKR/Gross murine leukemia virus (MuLV). Our published work has shown that this nonresponsive state is specific and not due to clonal deletion or irreversible functional inactivation of antiviral CTL precursors. In the present study, an alternative mechanism based on the presence of inhibitory AKR.H-2b cells was examined. Irradiated or mitomycin C-treated AKR.H-2b spleen cells function as in vitro stimulator cells in the generation of C57BL/6 (B6) anti-AKR/Gross virus CTL, consistent with their expression of viral antigens. In contrast, untreated viable AKR.H-2b spleen cells functioned very poorly as stimulators in vitro. Viable AKR.H-2b spleen cells were also able to cause dramatic (up to > or = 25-fold) inhibition of antiviral CTL responses stimulated in vitro by standard AKR/Gross MuLV-induced tumor cells. This inhibition was specific: AKR.H-2b modulator spleen cells did not inhibit allogeneic major histocompatibility complex-specific CTL production, even when a concurrent antiviral CTL response in the same culture well was inhibited by the modulator cells. These results and those of experiments in which either semipermeable membranes were used to separate AKR.H-2b modulator spleen cells from AKR/Gross MuLV-primed responder cells or the direct transfer of supernatants from wells where inhibition was demonstrated to wells where there was antiviral CTL responsiveness argued against a role for soluble factors as the cause of the inhibition. Rather, the inhibition was dependent on direct contact of AKR.H-2b cells in a dose-dependent manner with the responder cell population. Inhibition was shown not to be due to the ability of AKR.H-2b cells to function as unlabeled competitive target cells. Exogenous interleukin-2 added at the onset of the in vitro CTL-generating cultures partially restored the antiviral response that was decreased by AKR.H-2b spleen cells. Positive and negative cell selection studies and the development of inhibitory cell lines indicated that B lymphocytes and both CD4- CD8+ and CD4+ CD8- T lymphocytes from AKR.H-2b mice could inhibit the generation of AKR/Gross virus-specific CTL in vitro. AKR.H-2b macrophages were shown not to be required to demonstrate AKR/Gross MuLV-specific inhibition, however, confirming that the inhibition by T-cell (or B-cell)-depleted spleen populations was dependent on the enriched B-cell (T-cell) population per se.(ABSTRACT TRUNCATED AT 250 WORDS)

AKR murine leukemia virus↗

PubMed1996

Antibody to the ligand for CD40 (gp39) inhibits murine AIDS-associated splenomegaly, hypergammaglobulinemia, and immunodeficiency in disease-susceptible C57BL/6 mice.

Infection of genetically susceptible C57BL/6 mice with the LP-BM5 isolate of murine retroviruses cause profound splenomegaly, hypergammaglobulinemia, lymphadenopathy, and an immunodeficiency syndrome which includes the development of terminal B-cell lymphomas. Because many of these and the other manifestations of LP-BM5 virus-induced disease are similar to those seen in AIDS, this syndrome has been named murine AIDS, or MAIDS. Previous reports have shown that the onset of MAIDS depends on the presence of both CD4+ T cells and B cells and have suggested that CD4+ T-cell-B-cell interactions are important to disease pathogenesis. Here, we assessed the possibility that interactions between CD40 and its ligand on activated CD4+ T cells, CD40 ligand/gp39, are involved in the development of MAIDS. To test this hypothesis, LP-BM5-infected B6 mice were treated in vivo with anti-gp39 monoclonal antibody. As a result, MAIDS-associated splenomegaly, hypergammaglobulinemia, germinal center formation, and the loss of in vitro responsiveness to the T- and B-cell mitogens concanavalin A and lipopolysaccharide were inhibited. Anti-gp39 monoclonal antibody-treated LP-BM5-infected mice were also able to mount essentially normal alloantigen-specific cytolytic T-lymphocyte responses. These results support the possibility that molecular interactions between CD40 and gp39 are critical to the development of MAIDS.

AIDS-Related Complex↗