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Biomedical subjects

L Layward

Publications and source records attributed to L Layward.

30 records · Page 2Linked to original sources
PubMed1981

Long-term abnormalities in T and B lymphocyte function in children following treatment for acute lymphoblastic leukaemia.

T and B lymphocyte function as assessed by pokeweed mitogen stimulation and concanavalin A suppression was studied in 40 children with acute lymphoblastic leukaemia who were in remission and off all treatment. Both plasma cell and immunoglobulin production was reduced in off-treatment patients, particularly in those who had received cyclophosphamide as part of their treatment. The ability to suppress immunoglobulin production was also significantly reduced in these patients. These abnormalities were long-standing and were apparent up to 5 years after stopping treatment with no indication of a return to normality. No clinical correlations have been observed.

Adolescent↗
PubMed1981

Growth of pre-B cells in cultures of bone marrow from children with acute lymphoblastic leukaemia and other diseases.

Pre-B cells from the bone marrow of children with acute lymphoblastic leukaemia (ALL) survived up to 144 hr after the completion of treatment and divided in culture with maximum cell numbers at 24 hr. There was no rise in B cell number and no evidence of differentiation from pre-B to B cells. Binucleated pre-B cells in cultures containing cytochalasin B confirmed that pre-B cell division was occurring. Cycloheximide reduced cell numbers in culture but bromodeoxyuridine did not. Pre-B cell numbers also increased in culture of morphologically normal marrows from treated and untreated patients with solid tumours, and probably in normal marrows from patients with non-malignant diseases.

Adolescent↗
PubMed1981

T lymphocyte mobility: defects and effects of ascorbic acid, histamine and complexed IgG.

T lymphocyte mobility is low in patients with low neutrophil mobility. Thymocytes move comparably with normal mature T lymphocytes. Histamine accelerates T lymphocyte mobility in healthy subjects, patients with defective lymphocyte mobility and thymocytes. Ascorbic acid increases lymphocyte mobility of healthy subjects and thymocytes. Inhibition of mobility of T- or Tmu-depleted T lymphocytes by complexed IgG casts doubt on previous reports that the T gamma cells do not move.

Adult↗
PubMed1981

Increase and inhibition of pre-B cell proliferation in culture, by T cells.

T cells may either increase or decrease in vitro proliferation of marrow pre-B cells from patients with acute lymphatic leukaemia after withdrawal of successful treatment. There is less proliferation when T cells are removed by E rosetting, and repletion of T cells restores proliferation. When additional T cells from the patients were added to the patients' marrows, proliferation was increased more effectively than with T cells from healthy subjects; there was no evidence of an allogeneic effect. In contrast, normal T cells stimulated with concanavalin A suppress proliferation. There was no evidence of differentiation into B cells.

Adolescent↗
PubMed1979

Four families with immunodeficiency and chromosome abnormalities.

Six children, with severe deficiency of some or all of the immunoglobulins and minor somatic abnormalities, had chromosomal abnormalities: (1) 45,XY,t(13q/18q), (2) 46,XY,21ps +, (3) two brothers 46,XY (inv. 7) (4) 45,X,t(11p/10p)/46X,iXq,t(11p/10p) and, (5) in addendum, 45,XX,-18;46,XX, r18. The chromosome abnormalities were detected in B- as well as T-lymphocytes (as evidenced by using both PHA- and PWM-stimulated cultures) in all probands, but one was mosaic in PHA culture, although all his PWM-stimulated cells were abnormal. Chromosomal variants were also detected in relatives of three and immunodeficiency in relatives of two.

Agammaglobulinemia↗
PubMed1979

Maternal smoking and cord blood immunity function.

Thymidine uptake in PHA-stimulated culture of cord blood cells from smoking mothers is greater than that from non-smoking mothers. There was no such difference when separated lymphocytes were studied; this suggests that smoking suppresses a suppressor cell. No difference was detected in haemoglobin, immunoglobulins, transferrin, cell counts, E-rosette counts and leucocyte mobility.

Female↗
PubMed1978

Fc-receptor heterogeneity of human suppressor T cells.

Concanavalin A (Con A) stimulated the IgM-binding subpopulation of human T cells (TM) to suppress the pokeweed mitogen-induced differentiation of B lymphocytes to plasma cells. Control TM cells that had not been Con A activated did not suppress. The degree of suppression was related to the number of Con A-TM cells added to the cultures and it was abolished by irradiation of the T lymphocytes either before or after the 24-hr culture period with Con A. Suppression did not require the presence of TG cells, whose suppressor potential has been previously established. These findings indicate that suppressor activity is not confined to the TG subpopulation but may be expressed by TM cells also.

B-Lymphocytes↗
PubMedDate not supplied

Response to mucosal antigen challenge in IgA nephropathy.

While IgA nephropathy (IgAN) is characterized by the deposition of glomerular IgA, the source of the deposited IgA is not known, with both the mucosal and systemic IgA systems being implicated. In order to investigate mucosal and systemic antibody production to mucosal antigen challenge in IgAN, 9 patients and 11 controls were immunized intranasally with tetanus toxoid (TT). There was no significant difference in the serum or saliva IgG, IgA, IgA1, or IgA2 antibody production to TT. However, in IgAN there was an increase of in vitro IgA anti-TT production in Epstein-Barr virus transformed cultures of peripheral blood lymphocytes taken after mucosal immunization. This increase in traffic of immunocompetent cells between the systemic and mucosal systems could play a role in the link between the mucosa and glomerulus in IgAN. Systemic immunization with TT following mucosal priming did not result in any difference in the antibody response between patients and controls. There was no evidence from this study that mucosal immunization results in an enhanced antibody response in IgAN or that mucosal priming alters the subsequent systemic antibody response.

Administration, Intranasal↗
PubMedDate not supplied

In vitro immunoglobulin isotype suppression in immunoglobulin A nephropathy.

IgA nephropathy (IgAN) is characterized by mesangial IgA deposition, and up-regulation of the IgA system is frequently described. This study investigated in vitro immunoglobulin isotype production by peripheral blood mononuclear cells from patients with IgAN and controls, without mitogenic stimulation and under the influence of cell cycle inhibitors and cyclosporin A (CyA). In controls, only IgM production was suppressed by cell cycle inhibitors, and no isotype was affected by CyA. This suppressible IgM production may represent antigen-independent 'natural antibody'. In IgAN, IgM, IgA and IgG were all suppressed by cell cycle inhibitors, and CyA suppressed IgA production. This state of altered immune activation in IgAN demonstrates T-cell-independent IgA production, suggesting that it is IgA 'natural antibody'. In conclusion, we suggest that mesangial IgA deposition may not be antigen dependent but due to some non-immune characteristic of the IgA molecule.

Adult↗
PubMedDate not supplied

Increased IgA and decreased IgG production by Epstein-Barr virus transformed B cells in culture in IgA nephropathy.

Despite many studies describing IgA upregulation both in vivo and in vitro in IgA nephropathy (IgAN), the underlying mechanism of increased IgA production is not known. In this study, Epstein-Barr virus was used to transform B cells in vitro in a T-cell-independent manner in order to investigate immunoglobulin production by B cells in IgAN. B cells from patients with IgAN produced more IgA and less IgG in culture than controls. While both IgA subclasses contributed to the increase in IgA production, only IgA1 synthesis was significantly higher than controls. These results of increased IgA production in patients with IgAN, with a concomitant decrease in IgG production, demonstrate hyperactivity of B cells restricted to the IgA isotype in IgAN.

Adolescent↗