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Biomedical subjects

D A Cooper

Publications and source records attributed to D A Cooper.

At least 325 records · Page 18Linked to original sources

The immunological basis of immediate hypersensitivity.

IgE is a homocytotropic antibody which binds to the surface of the mast cell. Antigen with affinity for IgE triggers conformational change at the cell surface, resulting in the release of chemical mediators from the mast cell granules. The mediators histamine, slow reacting substance of anaphylaxis and eosinophil chemotactic factor cause smooth muscle contraction, increased capillary permeability, eosinophil attraction and increased glandular secretions. The release of mediators from the mast cell granules is controlled by intracellular levels of cyclic nucleotides. In particular, elevated cyclic AMP inhibits mediator release. Adrenergic, cholinergic and prostaglandin receptors all influence mediator release. The characteristic immunopathology of immediate hypersensitivity reactions is a result of local or systemic mediator release. Such reactions include anaphylaxis, asthma, allergic rhinitis, urticaria and angioedema. Similar immunopathology may sometimes result from mechanisms not involving IgE or histamine mediators. Routine investigation of patients with immediate hypersensitivity should include eosinophil counts and IgE levels in blood and secretions, and immediate hypersensitivity skin tests. RAST testing is not routine. Therapeutic principles of these reactions include restoration of inhibitory levels of cyclic nucleotides, antagonism of mediator effects and immunological manipulation of the IgE mediated allergic reaction.

Adrenal Cortex Hormones↗

Lymphoproliferative disease with IgM lambda monoclonal protein and autoimmune hemolytic anemia. A report of four cases and a review of the literature.

Four patients with lymphoproliferative disease with immunoglobulin M lambda (IgMlambda) monoclonal proteins and severe autoimmune hemolytic anemia are described. These patients had many features in common that may warrant their recognition as a specific entity within the lymphoproliferative spectrum. In each case, a wide thermal range low titer cold agglutinin was present. The association of cold autoimmune hemolytic anemia with IgMlambda monoclonal protein and lymphoproliferative disease is unusual. The literature on IgM monoclonal proteins associated with lymphoproliferative disease is reviewed with emphasis on the presence of direct antiglobulin test positive autoimmune hemolytic anemia.

Adult↗

The effect of acute and prolonged administration of prednisolone and ACTH on lymphocyte subpopulations.

The effect of acute and prolonged three week administration of prednisolone and ACTH on the numbers and function of T- and B-lymphocyte subpopulations in patients requiring corticosteroid therapy was studied. Prednisolone caused severe reduction in E-rosette-forming lymphocytes, phytohaemagglutinin response, EAC-rosette-forming lymphocytes and surface-membrane mu-positive B-lymphocytes maximal at 4--6 hr after administration with reversal sometimes to supernormal levels by 24 hr. Prolonged administration resulted in a similar pattern of response. Acute but not prolonged prednisolone administration caused a reduction in the percentage of E-rosette-forming lymphocytes maximal at 4 hr. ACTH caused moderate reduction in these parameters at 4 and 6 hr which remained low at 24 hr after prolonged administration.

Adrenocorticotropic Hormone↗

Monitoring immune function during immunosuppressive therapy.

Twenty-nine patients with a variety of connective tissue disorders were studied for the effects of immunosuppressive therapy on non-specific parameters of immune function. Baseline studies prior to therapy showed a frequent incidence of anergy (13%) lymphopenia (31%) and abnormal PHA response (43%). Despite these abnormalities in untreated patients it was possible to show an even higher incidence of anergy (31%), lymphopenia (66%) and abnormal PHA response (77%) following immunosuppressive treatment. The changes in lymphocyte count and PHA response were found to be statistically significant. It was found, paradoxically, that delayed hypersensitivity responses improved following institution of therapy in three patients. Clinical efficacy of immunosuppression correlated with lymphopenia and depressed PHA responses; in particular in the five patients with uncontrolled disease, these parameters were normal. Lymphocyte counts and PHA responses are the most simple and informative procedures to monitor immunosuppression in patients.

Collagen Diseases↗

T and B cell populations in blood and lymph node in lymphoproliferative disease.

Lymph node and peripheral blood lymphocytes were studied simultaneously for surface markers of T and B cells in 22 patients with lymphoproliferative diseases and 8 patients with non-neoplastic lymphadenopathy. This resulted in the classification of the malignancy from involved lymph nodes into 4 groups. Six patients had B cell lymphomata with normal or strong immunofluorescent staining for surface membrane immunoglobulin; 8 patients had B cell chronic lymphocytic leukaemia with pale staining for surface membrane immunoglobulin; 5 patients had T cell lymphomata and 3 patients were not definitely classifiable. In 6 out of 8 patients with B cell CLL, histopathology of lymph nodes showed infiltration with well differentiated lymphocytes and in all T cell lymphomata, the infiltrating cells were poorly differentiated. By the use of these markers, malignant lymphocytes were identified in the circulation in only 3 out of 6 patients with B cell lymphoma, in all patients with B cell CLL but in none of those with T cell lymphoma or unclassifiable lymphoma. Therefore a more conclusive characterization of the malignant lymphocyte in lymphoproliferative diseases must include an examination of involved lymph nodes.

B-Lymphocytes↗