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Biomedical subjects

E Luckhurst

Publications and source records attributed to E Luckhurst.

9 recordsLinked to original sources
PubMed1985

The role of alpha 1-antitrypsin deficiency in the pathogenesis of immune disorders.

The association between alpha 1-antitrypsin (alpha 1-AT) deficiency and a number of immune mediated diseases including rheumatoid arthritis, anterior uveitis, systemic lupus erythematosus, and asthma suggests that alpha 1-AT may be important not only as an anti-inflammatory protein but also as an immune regulator. That the relationship between decreased amounts of this inhibitor and these diseases is causal is suggested by both some of its physical properties and evidence indicating it is able to modulate immune function. alpha 1-Antitrypsin has a high plasma concentration, very broad range of inhibitory activity and is an acute phase reactant. Among other things, it is able to modulate lymphocyte proliferation and cytotoxicity, and monocyte and neutrophil function. Additionally, some of these changes are demonstrable in vivo in patients with severe alpha 1-antitrypsin deficiency. This paper reviews the important physicochemical characteristics of this protein, the association of its presence in decreased amounts with immune disorders, and finally the important mechanism that may underlie this disease association.

Connective Tissue Diseases↗
PubMed1977

Depressed lymphocyte function after bereavement.

During 1975 twenty-six bereaved spouses took part in a detailed prospective investigation of the effects of severe stress on the immune system. T and B cell numbers and function, and hormone concentrations were studied approximately 2 weeks after bereavement and 6 weeks thereafter. The response to phytohaemagglutinin was significantly depressed in the bereaved group on the second occasion, as was the response to concanavalin A at 6 weeks. There was no difference in T and B cell numbers, protein concentrations, the presence of autoantibodies and delayed hypersensitivity, and in cortisol, prolactin, growth hormone, and thyroid hormone assays between the bereaved group and the controls. This is the first time severe psychological stress has been shown to produce a measurable abnormality in immune function which is not obviously caused by hormonal changes.

Adult↗
PubMed1977

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↗
PubMed1977

Eosinophilia. V. Delayed hypersensitivity, blood and bone marrow eosinophilia, induced in normal guinea-pigs by adoptive transfer of lymphocytes from syngeneic donors.

Dinitrochlorobenzene (DNCB) induced delayed hypersensitivity but no eosinophilia in guinea-pigs from two colonies. Citraconic anhydride (CA) induced delayed hypersensitivity and eosinophilia of the blood and bone marrow, and sites of skin tests were also infiltrated by eosinophils. In adoptive transfer of lymphocytes separated from peritoneal exudate cells of strain XIII-sensitized donors, lymphocytes from DNCB-sensitized guinea-pigs transferred antigen-specific delayed hypersensitivity; lymphocytes from CA-sensitized guinea-pigs transferred delayed hypersensitivity, and induced eosinophilia of the blood and bone marrow of the recipients. Treatment of the lymphocytes before transfer with antilymphocyte (thymocyte) globulin or puromycin suppressed the manifestations in the recipients; normal globulin did not. Active sensitization with DNCB induced formation of small amounts, and with CA larger amounts of anaphylactic antibody. Sera from the actively sensitized animals elicited no significant eosinophilia of blood or bone marrow in one group of recipients. Passive anaphylaxis elicited a transient eosinophilia of the blood, but not of the bone marrow. It is postulated that T-helper cells interact with B-lymphocyte precursors, particularly IgE B cells, to stimulate eosinopoeisis. This results in a reserve of mature eosinophils that may be released in any subsequent anaphylactic event.

Anaphylaxis↗
PubMed1975

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↗
PubMedDate not supplied

Cell free serum interleukin-2 receptor levels after heart transplantation.

The aim of this study was to predict episodes of rejection or infection in heart transplant recipients by monitoring serum interleukin-2 receptor (IL-2R) levels, rather than by endomyocardial biopsy. The shedding of IL-2R from activated lymphocytes results in increased serum interleukin-2 levels and is probably a result of immune activation occurring in both rejection and infection processes. As a group, heart transplant recipients who had no rejection of infection had significantly increased serum IL-2R levels compared with healthy controls. Patients who had moderate and severe rejection, and infection, had significantly increased serum IL-2R levels compared with levels in patients without rejection or infection. High serum IL-2R levels were seen mainly within the first 3 months after transplantation. Of 15 patients studied, nine had consistent increases in serum IL-2R levels with episodes of rejection or infection. Serum IL-2R levels did not correlate with serum cyclosporine levels. The monitoring of serum IL-2R levels was not a sensitive test of rejection because increases were not seen in all episodes of rejection; increases were seen, however, in all cases of infection. This test lacked specificity as serum IL-2R levels increased during episodes of both rejection and infection. In conclusion, the monitoring of serum IL-2R levels may be a useful way to routinely monitor or screen for possible rejection infection in heart transplant recipients, but this method should not replace endomyocardial biopsy for diagnosing rejection.

Graft Rejection↗