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Biomedical subjects

S Schatten

Publications and source records attributed to S Schatten.

12 recordsLinked to original sources
PubMed1997

Autoimmune progesterone dermatitis: onset in a women without previous exogenous progesterone exposure.

Autoimmune progesterone dermatitis is a rare clinical entity that may be seen by the family practitioner, gynecologist, or dermatologist. Recognition of the entity is paramount in the therapy of this easily treated condition. We report a case of a 36-year-old woman with a recurrent facial dermatitis of many months' duration. We found the cutaneous eruption to be temporally related to her menstrual cycle. The patient denied any changes in her diet, cosmetics, medications, or soaps that could account for the dermatitis. Despite no previous exposure to exogenous progesterone, the diagnosis of autoimmune progesterone dermatitis was made. The patient was cured by oophorectomy.

Adult↗
PubMed1989

Vaso-occlusive retinopathy associated with antiphospholipid antibodies (lupus anticoagulant retinopathy).

The authors observed three cases (6 eyes) of vaso-occlusive retinopathy associated with the lupus anticoagulant and the related antiphospholipid antibody anticardiolipin. The disease occurred in patients who had no definable autoimmune disease such as systemic lupus erythematosus (SLE) and was characterized by severe bilateral retinal vascular occlusion. There was profound visual loss from intraretinal ischemia as well as vitreous hemorrhage from preretinal neovascularization. Results of laboratory testing showed a prolonged partial thromboplastin time (PTT) in two patients, and the presence of the lupus anticoagulant in all. Treatment with panretinal photocoagulation appeared to stabilize the neovascularization. The role of systemic anticoagulation and immunosuppressive therapy is uncertain.

Adult↗
PubMed1988

Treatment. Disease-modifying therapies.

Many patients with systemic lupus can be treated effectively with antimalarials and nonsteroidal anti-inflammatory drugs without ever having to take systemic corticosteroids at all or for any significant length of time. On the other hand, some patients with life-threatening disease, active major organ disease, or intolerable corticosteroid toxicities should be given immunosuppressive drugs, plasmapheresis, and/or other therapies in addition to corticosteroids early in their disease course, before permanent, end-organ damage occurs and before the predictable serious and debilitating toxicities of prolonged, daily high-dose corticosteroids develop. Just as lupus patients now routinely undergo detailed serologic testing, it is conceivable that, in the future, routine determination of human leukocyte antigen (HLA) haplotypes45 and T-cell subsets88a will help define, at disease onset, those patients who are destined to have severe disease. Perhaps this knowledge, combined with a better understanding of the exact mechanisms of action of these disease-modifying therapies, will allow a more rational approach to the treatment of SLE.

Antibodies↗
PubMed1984

Monoclonal antibodies to tissue-specific cell surface antigens. I. Characterization of an antibody to a prostate tissue antigen.

Monoclonal antibodies were raised to PC-3 human prostate adenocarcinoma cells, and one hybridoma, designated F77-129, was extensively purified and used to characterize a PC-3 antigen. The F77-129 antibody also showed serological reactivity with the Du-145 prostate cancer line and with three of four breast carcinoma lines tested; it showed variable binding to a colon carcinoma line. Several other lines tested, including melanomas, fibrosarcomas, and leukemias, were completely negative. Immunoperoxidase staining of frozen surgical specimens showed binding to both normal and malignant prostate and breast tissue. Injection of radioiodinated F77-129 into tumor-bearing nude mice showed specific in vivo targeting to prostatic cancer implants. The antigen also showed surface modulation by bound antibody, suggesting possible clinical utility of this antibody in delivering immunotoxins to tumors.

Adenocarcinoma↗
PubMed1984

Suppressor T cells and the immune response to tumors.

In this paper we have attempted to define the role of suppressor T cells in many well-defined murine tumor systems. We have knowingly omitted a blocking antibodies, suppressor B cells as mediators of tumor immunosuppression in various murine tumor systems; these have been well reviewed elsewhere. Also, we have focused on the importance of two different types of antigen-presenting cells in the induction and suppression of cell-mediated immunity and on some of the different modalities employed to inhibit Ts function. Finally, we have discussed the acquired immunodeficiency syndrome and the possible role of a defective helper pathway and enhanced suppressor pathway in its pathogenesis. We and others believe that the suppressor pathway is preferentially activated by tumor antigen(s) in the cases of many immunogenic murine tumors--possibly due to the release of tumor antigen(s) from tumor cells, their subsequent trafficking to specific areas of the spleen and other organs, and, ultimately, their presentation by certain APC to Ts. Ts may then act directly upon helper Lyt 1+2- T cells as these cells interact with tumor antigen(s) on I-A+ APC. Alternatively, if the effector pathway were somehow impaired--e.g., by ultraviolet radiation or a virus--then the suppressor pathway may be activated in an unregulated manner, often to the detriment of the host. Biochemical characterization of the tumor antigens that stimulate Ts generation and, presumably, tumor growth and definitive documentation of a role of APC in the processing and presentation of these tumor antigens to Ts need to be done. Then selective stimulation of the effector immune response, along with inhibition of the suppressor response, to tumor antigens with drugs, monoclonal antibodies, and soluble mediators or their analogues may be possible in the near future.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Regulation of the immune response to tumor antigens. X. Activation of third-order suppressor T cells that abrogate anti-tumor immune responses.

The experiments described further define the suppressor T cell pathway in the S1509a tumor system. We demonstrated previously that S1509a-induced Ts1, TsF1, and Ts2 specifically suppress in vivo Ly1+2- T cell-dependent responses to S1509a and that Ts1 suppress in vivo Ly-1+2- T cell-mediated proliferative responses to S1509a. We have now shown that in vivo administration of either S1509a-induced TsF1 or TsF2 suppresses both in vivo and in vitro Ly-1+2- T cell-mediated responses to S1509a. Furthermore, we revealed the existence of Ts3, which are activated by S1509a tumor antigen and TsF2, in this murine tumor system. Finally, we demonstrated that cyclophosphamide abrogates the suppressive effect of TsF2 but not that of Ts3. These results are discussed with respect to T cell-mediated suppression in other murine tumor systems and the possible pivotal role for a tumor antigen-presenting cell in activating Ts3 in the S1509a tumor system.

Animals↗
PubMed1984

Differential antigen presentation in tumor immunity.

The tumor S1509a elicits a cell-mediated immune response in immune A/J mice but leads to the generation of suppressor T cells (Ts) in nonimmune mice. Previous studies have shown that I-A+ antigen-presenting cells (APC) present S1509a tumor antigen and thereby activate immune T cells. Recent studies with polyoma-induced tumors reveal similar findings. Administration of anti-I-A antibodies not only prevents effective T cell activation by I-A+ APC bearing S1509a tumor antigen but also induces Ts after a tumor challenge. Ts, which inhibit S1509a tumor immunity, may be activated by tumor antigen presented on I-J+ APC. Examination of the immunologic effects of cyclophosphamide and UV radiation supports this hypothesis.

Animals↗
PubMed1983

Regulation of the immune response to tumor antigens. IX. In vitro Lyt-1+2- cell proliferative responses to cellbound or subcellular tumor antigen.

We investigated the cellular basis of immune reactivity to the S1509a fibrosarcoma in tumor-immune A/J mice. In a Winn assay, immune Lyt-1+2- T cells are capable of retarding S1509a tumor growth in naive A/J mice. In vitro proliferation to S1509a is also mediated by tumor-immune Lyt-1+2- T cells. This response is specific to the immunizing tumor and appears 5 to 7 days after reexposure to the tumor in vivo. Proliferation also requires the presence of a population of adherent cells. In fact, adherent peritoneal exudate cells pulsed with tumor membrane fragments derived from S1509a cells can stimulate proliferation. Proliferation is blocked by the addition of anti-I-Ak monoclonal antibody to the culture medium without complement or by treatment of the responder population with anti-I-Ak and complement. In vitro responsiveness is also inhibited by the presence of tumor-specific suppressor T cells in vivo. These observations suggest in vitro proliferation may provide a potential means of defining tumor antigens and cell-surface structures involved in tumor immunity.

Animals↗
PubMed1983

Inhibition of tumor growth by monoclonal anti-I-J antibodies.

In this paper we have examined the effects of i.v. administered monoclonal anti-I-J antibodies on tumor growth in syngeneic and semi-syngeneic hosts. These antibodies inhibit tumor growth in mice bearing the appropriate I-J-encoded gene product on their lymphoid cells at nanogram dosages. The spleens of monoclonal anti-I-J-treated primary tumor-bearing mice do not contain transferable tumor-specific cells. These findings suggest that inhibition of suppressor cell function may be the mechanism by which anti-I-J antibodies inhibit tumor growth. We have also demonstrated that tumors growing in F1 hybrid mice are inhibited by monoclonal anti-I-J antibodies reactive with either parental haplotype and that there is no evidence of synergy when both antibodies are administered simultaneously. This may indicate that I-J molecules are codominantly expressed on a critical component of the F1 suppressor pathway.

Animals↗