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Biomedical subjects

A Basten

Publications and source records attributed to A Basten.

At least 163 records · Page 9Linked to original sources
PubMed1978

The successful treatment of primary amyloidosis with intermittent chemotherapy.

A patient with primary amyloidosis is described with extensive vital organ involvement including infiltration of the liver, kidney and myocardium. Treatment with intermittent melphalan and prednisone resulted in improved hepatic and renal function, a reduction in liver size and arrested amyloid deposition in the myocardium. These observations suggest that chemotherapy can halt tissue amyloid deposition, and improve the prognosis of primary amyloidosis.

Adult↗
PubMed1977

HLA and bird breeder's hypersensitivity pneumonitis.

HLA antigen status was assessed in non-related individuals and related family members with bird breeder's hypersensitivity pneumonitis (HP). 35% of 20 non-related patients carried HLABW40 compared to 10% of 861 normal controls (p less than 0.001, Pc less than 0.05, respectively). A consistent association of an HLA haplotype with disease was demonstrated in three of four families. Selected HLA antisera contained antibodies which blocked the blastogenic response to bird antigen. This study suggests the existence of an HLA associated Ir gene in bird breeder's HP.

Alveolitis, Extrinsic Allergic↗
PubMed1976

Myocardial infarction in Wegener's granulomatosis.

A case is described of a 28-year-old man who presented with a picture of classical Wegener's granulomatosis; and who, in the absence of fulminating renal or respiratory disease died from myocardial infarction. Other reports of cardiac involvement are discussed and compared with the picture presented by this patient.

Adult↗
PubMed1976

A receptor for antibody on B lymphocytes. III. Relationship to immunoglobulin and ia determinants.

The physicochemical structure of the receptor for antibody (FcR) on B cells and its interrelationship with Ig and H-2 gene complex associated antigens were examined. FcR were found to be sensitive to treatment with phospholipase C and pronase, but resistant to neuraminidase, phospholipase A and chymotrypsin. They would therefore appear to be composed of phospholipoproteins. Several lines of evidence indicated that FcR and Ig receptors were discrete entities: thus, FcR (1) were resistant to chymotrypsin; (2) capped independently of Ig, as demonstrated by means of Fab fragments of anti-Ig, and (3) were closely associated with at least some Ia determinants, which are known to be distinct from Ig determinants. The relationship between FcR and H-2 gene complex associated antigens was confirmed by demonstrating inhibition of binding of aggregates by anti-Ia serum and vice versa. If, however, FcR were capped, anti-Ia serum applied under non-capping conditions was still found to bind diffusely to the great majority of B cells. Although this could be explained in part by the presence of residual FcR, some Ia determinants appeared to be distinct from FcR. The finding of residual FcR after capping with aggregates or immune complexes implied that FcR are a more integral part of the cell membrane than Ig receptors and could therefore act as proreceptors for the latter. Consistent with this was the demonstration of a significant polar distribution of Ig on B cells capped for FcR and then labelled under non-capping conditions with anti-Ig.

Animals↗
PubMed1975

Cellular basis for the immune response to methylcholanthrene-induced tumors in mice. Heterogeneity of effector cells.

Immune resistance to methylcholanthrene-induced tumors has two phases, an early specific and a late non-specific phase. Both phases were found to be T-cell-dependent in vivo. Thus, adult thymectomized, irradiated, bone-marrow-protected mice bearing H-1 tumor isografts showed impaired resistance to challenge with homologous (H-1) and heterologous (H-3) tumor cells. In each case resistance was restored by injection of thymus cells. In vitro analysis of the cellular basis of resistance revealed that different mechanisms were involved in the two phases. The cytotoxic effect of immune spleen cells taken during the early specific phase was inhibited by pretreatment with anti-O serum and complement and by removal of macrophages. Neither procedure, however, interfered with the cytotoxic potential of immune spleen cells taken during the late non-specific phage of immunity. Passage of immune spleen cells through rabbit-IgG anti-mouse immunoglobulin-coated columns (which yielded a T-cell-enriched, B-cell-depleted population) resulted in abrogration of cytotoxicity whether the cells were obtained during the early or the late phase of resistance. The inability of late-phase spleen cells to kill was explicable in terms of B-cell removal since T-cells and macrophages had been shown to be ineffective at that time. In contrast, the failure of column-treated cells from the early phase to kill was found to be due to removal of adherent cells rather than B-cells since cytotoxicity (1) was abrogated by passage through control columns coated with rabbit-IgG anti-sheep red blood cell antibody which did not retain B-cells and (2) could be restored by addition of immune macrophages (from anti-O serum-treated spleens). Taken together, these results indicate that the cellular basis of immune resistance to methylcholanthrene-induced tumors is heterogeneous. The early specific phase seems to be mediated by an interaction between T-cells and macrophages; the late none-specific phase, although T-cell dependent in its induction, depends on a different effector mechanism, possibly involving a cell or its products of the B lineage.

Animals↗
PubMed1975

Relationship between Fc receptors, antigen-binding sites on T and B cells, and H-2 complex-associated determinants.

The relationship between H-2 complex-associated determinants, Fc receptors, and specific antigen-recognition sites on T and B cells was examined by binding and functional assays. The Fc receptor was detected by radiolabeled immune complexes or aggregated human IgG. Both these reagents selectively bound to B cells, not to T cells. When spleen cells, from mice primed to several antigens, were exposed to highly substituted radioactive aggregates, their capacity to transfer both a direct and indirect plaque-forming cell response to these antigens was abrogated. Addition of B cells, but not of T cells, restored responsiveness. Complexed Ig binding to Fc receptors was prevented by pretreatment of mixed lymphoid cell populations with antisera directed against membrane components on the same cell (e.g., H-2) and on other cells (e.g., theta). The lack of specificity of inhibition was thought to be due to the formation on cell surfaces of antigen-antibody complexes which would then attach to the Fc receptor during the incubation precedure. Specific blockade of the Fc receptor during the incubation procedure. Specific blockade of the Fc receptor however occurred when B cells were pretreated with the Fab fragments of anti-H-2 antibody. This was demonstrated autoradiographically and by inhibition of aggregate-induced suicide. The blocking activity of ante-H-2 Fab was removed by absorption with spleen cells from thymectomized irradiated mice but not with thymus cells of appropriate specificity. This suggested that the antibodies involved had specificity for determinants on the B-cell membrane distinct from those coded by the K or D end of the H-2 complex, and either absent from, or poorly represented on, thymus cells. Specific antigen-induced suicide of B cells was achieved simply by incubating the cells with radioactive antigen in the cold. T-cell suicide on the other hand required that the 125I-labeled antigen be presented to the T cells at 37 degrees-C on the surface of spleen cells from antigen-primed mice. Pretreatment of T cells with the Fab fragment of anti-H-2 antibody protected them from the suicide effect. By contrast no such protection of B cells could be achieved by this procedure. In other words H-2 (? Ir)-associated determinants may not only be in close proximity to the antigen-binding site on T cells but, in addition, may be involved in the effective operation of the receptor.

Animals↗
PubMed1975

Familial hypersensitivity pneumonitis.

Two families are described in which seven members of a total of 19 were found to have hypersensitivity pneumonitis due to exposure to avian antigens. Diagnosis was made on the basis of characteristic roentgenologic changes together with respiratory function and immunologic studies. The latter included screening for precipitins, macrophage migration inhibition (MMI) to specific antigens in avian serum and droppings, quantitation of immunoglobulin and alpha1 antitrypsin (AAT) levels and assessment of the complement system. Specific precipitins to pigeon and/or budgerigar serum were found in the serum of only four of the seven patients. Six of these seven patients, however, had a positive MMI. Thus, the MMI test, at least in this group of patients appeared to be a more sensitive indicator of active disease. The finding of seven members of two families with disease led to a search for predisposing factors, either genetic or environmental. Evidence for a genetic predisposition came from tissue typing studies. In the first family, both paternal haplotypes were associated with disease; the maternal haplotype HLA3,7 was not inherited by any child with disease. In the second family, the disease developed in three of four members with the haplotype HL-A2,W15, who were significantly exposed to avian antigen. In the light of recent studies showing an association between immune response (Ir) genes, histocompatibility antigens and disease susceptibility, these findings were interpreted as possible evidence for a subtle genetically linked immune defect in hypersensitivity pneumonitis. Evidence for an environmental predisposition was less clear cut, but it is interesting that members of both families used a gamma isomer of hexachlorobenzene (Nickoff) to eradicate mite infestations in their birds which might have damaged the bronchial mucosa or acted as an immunologic adjuvant in a person with underlying susceptibility to disease. The presence of subclinical respiratory disease in two family members is reported, and the importance of performing a range of investigations of respiratory function in order to detect disease and monitor its progress is emphasized.

Adolescent↗