Immune status and BCG vaccination in newborns with intra-uterine growth retardation.
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In severe intra-uterine growth retardation there are low IgG levels, low numbers of B cells and low percentage as well as numbers of T cells in cord blood. Following BCG vaccination given soon after birth, Mantoux conversion and leucocyte migration inhibition response to BCG was defective. (+info)
Rabbit lymphoid cells. II. Anti-allotype antisera, lipopolysaccharide and other bacterial and fungal mitogens as probes for the identification of B-cell subpopulations.
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Removal of adherent cells or complement-mediated killing of rabbit thymus lymphocyte antigen (BTLA) bearing rabbit T lymphocytes did not abolish the responsiveness (increased thymidine incorporation) of lymphoid cells to antibody against immunoglobulin allotype, Nocardia water-soluble mitogen (NWSM), pneumococcal polysaccharide SIII (PPSIII), S. abortus lipopolysaccharide (LPS), lipid A conjugated to bovine serum albumin and a crude preparation containing C polysaccharide from the cell wall of Diplococcus pneumoniae. Isologous and heterologous antisera, directed against different portions of the Ig receptor, differed in their capacity to enhance thymidine incorporation. The difference in mitogenicity of these antisera was discussed in terms of the accessibility of cell-bound immunoglobulin receptor sites. Spleen cells, responsive to anti-allotype (Ab4) antiserum and B-cell mitogens, NWSM and PPSIII, were characterized by velocity sedimentation. The mean volume of NWSM- and PPSIII-responsive cells was larger than that of the cells responsive to anti-allotype antiserum. Fractionation of spleen cells on glass bead columns yielded a population of non-adherent cells which were two to six times as responsive to anti-Ab4 antiserum as the original spleen cell suspension. The responsiveness of peripheral blood lymphocytes to anti-Ab4 antiserum was significantly greater than that of spleen cells. On the other hand, spleen cells were more responsive to PPSIII than were cells from the peripheral blood, the popliteal and the mesenteric lymph nodes. (+info)
Interactions between Mycoplasma pneumoniae and guinea pig complement.
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The "toxic" effect of guinea pig serum (GPS) on Mycoplasma pneumoniae cells was tested under various conditions, using rounding and killing of the cells as test systems. Both activities could be inhibited by heat inactivation (56 C, 30 min). Killing required both Ca2+ and Mg2+, rounding only Mg2+. Both activities were temperature dependent and no rounding or killing occurred at 4C. Incomplete complement sequences with natural of artificial defects in C1, C4, or C6 resulted in lost or reduced killing. The rounding activity was only slightly affected. Anti-C3 antiserum blocked both phenomena; incubation of GPS with 10 mg of inulin per ml reduced the rounding activity, and the same treatment of GPS deficient in C4 inhibited rounding totally. Properdin factor D was shown to be necessary for rounding by GPS, with defects in either C1 or C4. By immune adherence bound C3b could be demonstrated on M. pneumoniae cells after GPS treatment, no antibodies against M. pneumoniae could be found in GPS by immune fluorescence. The results give evidence for complement being the toxic factor in GPS. Efficient killing requires the intact complement sequence. Furthermore, M. pneumoniae cells are able to activate the alternate pathway of complement. Activation of this pathway results in rounding of the cells, which are partly able to recover after this reaction. Biological consequences for the mycoplasmas are death or damage and possibly opsonization, even in the absence of specific antibodies. The host, too, is possibly affected by products of the reaction. The interaction of M. pneumoniae and complement could be involved in the early stages of the development of M. pneumoniae disease. (+info)
Rosette-forming ability of thymus-derived lymphocytes in humoral and cell-mediated immunity. II. Helper cell activity.
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The technique of velocity sedimentation at unit gravity was used to determine the size and rosette-forming ability of helper cells in nonimmune and immune C57BL/6 mice. Helper T cells were assayed by the ability to cooperate with bone barrow (B) cells in the antibody response to sheep erythrocytes (SRBC) in vivo. 19S helper cells in nonimmune animals were nonrosette-forming small lymphocytes; after immunization with SRBC in complete Freund's adjuvant, 19S helper cells were nonrosette-forming medium lymphocytes. 7S helper cells in immune animals were small lymphocytes which did not form rosettes. No SRBC binding by helper cells was observed under the conditions of rosette formation used. (+info)
Separation of T lymphocytes from normal individuals and patients with B lymphocyte chronic lymphocytic leukaemia.
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Previous studies have shown that lymphocytes from patients with chronic lymphocytic leukaemia have a diminished response to mitogens which stimulate T cells. Chronic lymphocytic leukaemia is most often a disease of accumulating B cells so that T lymphocytes are diluted by large numbers of leukaemic cells. Direct comparison with the responses of normal lymphocytes to mitogenic stimulation is therefore suspect. To circumvent this difficulty, a method of isolating T cells from normal individuals and patients with chronic lymphocytic leukaemia was developed. Lymphocytes containing an average of 16.1 per cent B cells from normal individuals were applied to IgG-anti-IgG-coated Degalan bead columns and held at 4 degrees for 2 hours. The eluted cells contained less than 2 per cent B cells. When chronic lymphocytic leukaemic lymphocytes, containing an average of 68.6 per cent B cells, were applied to IgG-anti-IgG columns, the eluted cells contained 36.4 per cent B cells. To improve the purification of T lymphocytes, columns of uncoated Degalan beads were used to remove non-specifically adherent cells. Eluted lymphocytes were then applied to IgG-anti-IgG columns. This resulted in the recovery of purified populations of T cells with less than 2 per cent contamination with B cells. Patients with chronic lymphocytic leukaemia were found to have lymphocytes with either a normal density or a low density of surface immunoglobulins. B cells were successfully removed from lymphocyte suspensions in all cases of chronic lymphocytic leukaemia with a normal density of lymphocyte surface immunoglobulins. In the three cases of chronic lymphocytic leukaemia with low density surface immunoglobulins, separation by this method was unsuccessful. However, an enriched T-cell population was obtained when leukaemic lymphocytes which had lost all detectable surface immunoglobulins were passed through a column coated with heat-aggregated IgG. (+info)
Human T-cell heterogeneity as delineated with a specific human thymus lymphocyte antiserum. In vitro effects on mitogen response mixed leukocyte culture, cell-mediated lymphocytotoxicity, and lymphokine production.
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Human peripheral blood lymphocytes (PBL) were evaluated by their responses to phytohemmagglutinin (PHA-P), concanavallin A (con-A), and pokeweed mitogen (PWM), both before and after treatment with an antiserum against human thymic lymphocyte antigens (HTLA) that had been made T-cell-specific by multiple absorptions with immunoglobulin EAC-positive lymphoblast cell lines (B cells). Cells treated with HTLA were examined for their ability to react in a mixed lymphocyte culture (MLC) and to form killer cells in a cell-mediated lymphocytotoxicity (CML) system. Sensitized cells were also examined for their ability to respond to purified protein derivative (PPD) by blastogenesis, migration inhibitory factor release (MIP), and lymphotoxin (LT) production, both before and after treatment with HTLA and complement. The HTLA was in itself highly stimulatory to PBL. However, with the addition of complement and subsequent cell destruction, a marked decrease in its stimulatory response was noted. PBL treated with HTLA and complement exhibited marked inhibition of responsiveness to con-A with little decrease in PHA-P -OR PWM stimulation except at very high concentration of HTLA. MLC reaction was inhibited only when responder cells were treated with HTLA + C'. Treatment of stimulator cells with HTLA + C' did not significantly alter the MLC response. The HTLA + C'-treated cells failed to form killer cells in the CML reaction and inhibited PPD-induced blasto-genesis from PPD-sensitized individuals; however, treatment of sensitized cells with HTLA + C' had little effects on the release of MIF and LT. It is suggested that subpopulations of T-cells carry surface antigens that bind with this specific antisera, and that the con-A-responsive cells, the responder cells in the MLC, and killer T-cells comprise a separate subset from cells responding to PHA-P or PWM, OR THE MIF-and LT-producing cells. (+info)
Peripheral blood T and B lymphocytes during acute rheumatic fever.
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Proportions and total numbers of thymus-derived (T) and bone marrow-derived (B) peripheral blood lymphocytes were studied in 53 patients with acute rheumatic fever, diagnosed on the basis of modifified Jones criteria. An elevation in both proportions and absolute numbers of cells bearing surface Ig was found in most patients, particularly during the first 7 days after onset. Conversely, T-cell proportions and numbers were often found to be depressed early in the acue phases of rheumatic fever. Proportions of cells bearing surface Ig did not correlate with another B-cell marker, the aggregated gamma globulin receptor, suggesting that such cells bearing surface Ig were not all B lymphocytes. Incuvation for 20 h at 37 per cent C of cells showing high proportions of surface Ig-bearing surface Ig in both normal and rheumatic fever subjects, although there was no appreciable increment in proportions of lymphocytes expressing T-cell markers. Patients with initial attacks showed higher percentages and total numbers of Ig-bearing lymphocytes (P smaller than 0.01) than did those with rneumatic fever recurrences. Elevations in numbers and proportions of peripheral blood lymphocytes bearing Ig appeared to correlate with the relative acute nature of the rheumatic fever attack. (+info)
C3 receptors on direct plaque-forming cells.
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Using a rosette technique it is shown that only a small proportion of direct plaque-forming cells posses detectable C3 receptors 5 and 7 days after antigenic stimulation. The significance of this result is discussed. (+info)