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Biomedical subjects

J Leibowitch

Publications and source records attributed to J Leibowitch.

At least 37 records · Page 2Linked to original sources
PubMed1984

HTLV-III in cells cultured from semen of two patients with AIDS.

Epidemiological results suggest that the etiological agent of the acquired immune deficiency syndrome (AIDS) is transmitted primarily through blood products, semen, and saliva. There is evidence that the human T-cell leukemia (lymphotropic) virus type III (HTLV-III) is this agent. HTLV-III has been isolated repeatedly from T cells obtained from peripheral blood or lymph node tissue of AIDS and pre-AIDS patients and of healthy people believed to have been exposed to the virus. In the present study, HTLV-III was detected in and isolated from T cells present in the seminal fluid of AIDS patients. Mononuclear cells from the semen of AIDS patients and normal individuals were cultured in the presence of T-cell growth factor (interleukin-2). After 6 to 8 days, HTLV-III antigens were transiently expressed by the cells from the AIDS patients but not by those from the normal individuals. When the mononuclear cells from the semen of AIDS patients were cocultured with a permissive human T-cell line, cell cultures were produced that expressed high levels of reverse transcriptase activity, showed retroviral particles by electron microscopy, and were positive for HTLV-III-specific antigens when tested by fixed-cell indirect immunofluorescence with the use of monoclonal antibodies to the p24 and p15 antigens of HTLV-III.

Acquired Immunodeficiency Syndrome↗
PubMed1983

Isolation of human T-cell leukemia virus in acquired immune deficiency syndrome (AIDS).

Several isolates of a human type-C retrovirus belonging to one group, known as human T-cell leukemia virus (HTLV), have previously been obtained from patients with adult T-cell leukemia or lymphoma. The T-cell tropism of HTLV and its prevalence in the Caribbean basin prompted a search for it in patients with the epidemic T-cell immune deficiency disorder known as AIDS. Peripheral blood lymphocytes from one patient in the United States and two in France were cultured with T-cell growth factor (TCGF) an shown to express HTLV antigens. Virus from the U.S. patient was isolated and characterized and shown to be related to HTLV subgroup I. The virus was also transmitted into normal human T cells from umbilical cord blood of a newborn. Whether or not HTLV-I or other retroviruses of this family with T-cell tropism cause AIDS, it is possible that patients from whom the virus can be isolated can also transmit it to others. If the target cell of AIDS is the mature T cell as suspected, the methods used in these studies may prove useful for the long-term growth of these cells and for the identification of antigens specific for the etiological agent of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1981

Mechanism of action of the C4 nephritic factor. Deregulation of the classical pathway of C3 convertase.

Three mechanisms that regulate the formation and function of the classical pathway C3 convertase (C4b2a) have been elucidated: (a) an intrinsic decay of the enzyme that is temperature dependent; (b) an extrinsic decay mediated by the effect of the serum protein C4b binding protein (C4-bp); and (c) inactivation of C4b by the proteolytic action of C4b/C3b inactivator (C4b/C3bINA), which cleaves that alpha' chain of C4b to yield C4d (alpha 2) and C4c (alpha 3, alpha 4, beta, and gamma chains). A fourth mechanism described here is based on the observation that the IgG fraction of the serum of certain patients with glomerulonephritis contains a protein termed C4 nephritic factor (NFc), which prevents the intrinsic decay of C4b2a. This protein, which prolongs the half-life of surface-bound C4b2a from 7.5 min to greater than 5 h, increases the use of C3 and C5. It also inhibits the decay produced by C4-bp by preventing the dissociation of C2a from the C4b2a complex. Additionally, the C2b/C3bINA alone, or in the presence of C4-bp, fails to cleave the alpha' chain of C4b in the surface-bound stabilized C4b2a complex. This protective property of NFc requires the presence of C2a, because C4b was not protected unless it was bound to C2a. Thus in the presence of NFc, the three natural controls of the function of the classical pathway convertase, intrinsic decay, extrinsic decay, and proteolytic cleavage, are bypassed.

Animals↗
PubMed1981

[Immune complex nephropathy and hereditary deficiency of C1 esterase inhibitor (author's transl)].

Deficiency of C1 esterase inhibitor (C1-INH) was demonstrated in 7 of 22 subjects belonging to the same French family. Immune complex glomerulonephritis without lupic symptoms was discovered in one of the C1-INH deficient subjects, and in a girl of the same family the same deficiency was associated with an insulin-dependent diabetes of sudden onset. The pathophysiological consequences of complement deficiency resulting from the lack of C1 esterase inhibitor are discussed.

Adolescent↗
PubMed1981

Systemic lambda light-chain deposition in a patient with myeloma.

Systemic lambda light-chain deposition occurred in a 73-year-old man with myeloma. An initial renal biopsy specimen showed the features of myeloma kidney. When he died 22 months later lambda light chains were detected by immunofluorescence in kidneys, liver, spleen, and heart. They were probably responsible for cardiac dysfunction and the fatal arrhythmia. It is suggested that in this patient deposition was due to a structural alteration of the light chains, possibly induced by cyclophosphamide.

Aged↗
PubMed1981

Clq deposits at the dermoepidermal junction: a marker discriminating for discoid and systemic lupus erythematosus.

Discoid lupus (DL) and systemic lupus erythematosus (SLE) patients have been comparatively evaluated for complement and immunoglobulin deposits at the dermoepidermal junction (DEJ) by immunofluorescence (IF). When IF was positive, Clq deposits were quasi-constantly found in SLE patients with or without skin lesions (90%), while Clq was found in only 29% of the DL patients. Of the 42 DL patients followed-up to at least 2 years, 4 have eventually evolved a systemic disease. In these 4, neither cryoglobulinemia nor significant titers of ANA had been found at the time of presentation. Only 1 of these 4 patients had initially circulating immune complexes (P.E.G) and a positive IF in a normal sunprotected area. Clq deposits at the DEJ were present in all these 4. Of the remaining 38 DL patients, none has progressed to SLE: 8 had had significant titers of ANA, 5 had had circulating immune complexes, and 3 others had had cryoglobulinemia. Thus Clq deposits in DL cases are associated with a relatively high incidence of eventual systemic disease. Taken together, these data suggest that Clq deposits in skin may be a marker for systemic lupus.

Adolescent↗
PubMed1980

[Treatment of severe systemic lupus erythematosus. Long-term results in 55 patients (author's transl)].

Out of 55 patients with severe systemic lupus erythematosus (SLE) retrospectively studied from 1962 to 1979, 32 had diffuse proliderative glomerulonephritis and 23 had one or several extrarenal and/or haematological manifestations of the disease. All received corticosteroids in high dosage (0,8 to 1,5 up period was 48 months from the beginning of treatment. The actuarial survival rates for the whole groupe after 1,5 and 10 years were 92,4%, 83,4% and 77,2% respectively. Eight patients died: 5 of SLE and 3 of iatrogenic complications. Four are kept alive by maintenance haemodialysis. At the end of the study period, SLE was quiescent in 37 patients, including 14 who had discontinued corticosteroids for 5 to 72 months. The five-year survival rates were very similar in patients with renal and extrarenal involvement (86,4% and 81,6% respectively). In the latter group myocardial insufficiency, thrombopenia and thromboembolic complications were the main factors of morbidity and mortality. Corticosteroids were administered alone to 25 patients and in combination with cyclophosphamide to the remaining 30. Cyclophosphamide was given initially in 13 cases or subsequently on account of intolerance (7 cases) or resistance (10 cases) to steroids. Similar results were obtained with these two therapeutic regimens, but it must be noted that cyclophosphamide was mainly used in the more severe forms of SLE.

Adrenal Cortex Hormones↗