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C Henry

Publications and source records attributed to C Henry.

At least 145 records · Page 8Linked to original sources

Expression of the major cross-reactive idiotype in a primary anti-azobenzenearsonate response.

We have studied the occurrence of IgM plaque-forming cells secreting the cross-reactive idiotype (CRI) characteristic of the anti-azobenzenearsonate antibody responses in individual mice of different strains after one injection of the T-independent antigen, p-azobenzenearsonate-Brucella. Under these conditions of stimulation we find that idiotype is not unique to the Igh-1e and Igh-1d allotypes, but is expressed prominently in Igh-1a and Igh-1j strains and to a lesser but significant extent in Igh-1c and Igh-1b strains. We confirmed previous work that idiotype expression in mice hyperimmunized with protein conjugates of azobenzenearsonate is mainly restricted to mice of the Igh-1e allotype, but we find the display to be less marked than in mice given a single injection of the Brucella conjugate. We conclude that the B cell repertoire is inadequately revealed by analysis of serum antibodies of hyperimmune mice. We suggest the apparent correlation of the anti-azobenzenearsonate idiotype to allotype may be influenced by the activity of heavy chain regulatory genes, rather than the presence or absence of structural genes coding for the major CRI. We cannot exclude the possibility that the previously designated CRI-negative strains may express a cross-reactive determinant that is not necessarily a product of the CRI gene family.

Animals↗

Stimulation of human neutrophil chemiluminescence by soluble immune complexes and antibodies to neutrophils.

Activation of the neutrophil surface membrane may occur with a variety of stimuli, leading to enhanced glucose oxidation via the hexose monophosphate shunt and production of toxic oxygen radicals such as superoxide anion. This metabolic stimulation may be accompanied by light emission or chemiluminescence. The objective of these studies was to determine the effects of soluble and insoluble immune complexes, IgG aggregates, and rabbit anti-neutrophil serum on neutrophil activation as measured by chemiluminescence. Also, the uptake of immune complexes by neutrophils was determined and was correlated with the solubility of the complexes and the levels of induced chemiluminescence. The results indicate that stimulation of neutrophil chemiluminescence and uptake of immune complexes by neutrophils were both closely correlated with the percent precipitation of the immune complexes. Insoluble immune complexes that were avidly ingested by neutrophils also stimulated maximum levels of chemiluminescence. Nevertheless, elevated levels of chemiluminescence were induced by soluble immune complexes that were poorly ingested by neutrophils. Similarly, soluble aggregated IgG induced elevated levels of neutrophil chemiluminescence in a dose-dependent manner. Aggregated IgG induced up to sixfold higher levels of neutrophil chemiluminescence than did equal amounts of monomeric IgG. Finally, rabbit anti-neutrophil serum also caused increased levels of neutrophil chemiluminescence. Since previous studies have shown that sera from some patients with rheumatoid arthritis and Felty's syndrome have increased amounts of neutrophil-binding IgG due to the presence of both immune complexes and neutrophil-reactive antibodies, the effect of these sera on neutrophil chemiluminescence was studied. Positive correlations were observed between the level of neutrophil chemiluminescence induced by the sera and the amount of serum IgG neutrophil-binding activity (r = 0.72, p less than 0.001) as well as the level of immune complexes determined by C1q binding (r = 0.76, p less than or equal to 0.001). Such neutrophil activation by immune complexes or antibodies may reflect production of toxic oxygen radicals and could subsequently affect neutrophil function.

Antibodies↗

Role of membrane receptors in the induction of an in vitro secondary anti-hapten response. I. differentiation of B memory cells to plasma cells is independent of antigen-immunoglobulin receptor interaction.

In these experiments, we show that the interaction of antigen and B cell surface immunoglobulin is not essential for the generation of an IgG in vitro response to the hapten p-azophenyl-lactoside (lac). In our experimental system, keyhole limpet hemocyanin (KLH) was first selectively attached either to H-2, Ia or Ig receptors of lac-primed B cells by a hapten sandwich technique or to Fc receptors by complexes of azophenyl arsonate (ars)-coupled KLH and anti-ars. The labeled cells were then cultured with KLH-specific T cells for 5 days in the absence of antigen. Under all conditions of attachment we observed a significant anti-lac IgG response. We have demonstrated an absolute requirement for KLH-specific helper T cells. The results thus indicate that T helper cells are by themselves, regardless of the B cell antigen that serves to effect bridging, sufficient to activate B memory cells. We could find no evidence to support either a matrix theory or a two-signal hypothesis as currently proposed.

Animals↗

Role of membrane receptors in the induction of an in vitro secondary anti-hapten response. II. Antigen-immunoglobulin receptor interaction is not required for B memory cell proliferation.

In this study it has been investigated whether the interaction of antigen and B cell surface immunoglobulin (sIg) is required for full clonal expansion of memory B cells specific for the hapten, p-azophenyl-lactoside (lac). Cultures of lac-primed B cells and keyhole limpet hemocyanin (KLH)-specific T cells were activated in three ways: (a) by the antigen lac-KLH, (b) in the absence of lac epitopes by attaching KLH to the H-2 antigens of the B cells, and (c) in similar conditions where lac epitopes were supplied on carriers unrecognized by helper T cells. Dilution analyses showed that the yield of IgG anti-lac plaques per activated precursor was identical in all situations, and that the increased responses observed in the presence of lac epitopes were due to an increase in the frequency of activated precursors. Our results thus indicate that specific interacting T cells convey both the differentiative and proliferative signals to B memory cells, and are at variance with proposals advocating that an antigen-induced proliferative phase is succeeded by a T-cell-dependent differentiative event. We suggest that the effect of sIg-antigen interaction may be to cycle some precursors into a more easily activated state.

Animals↗

Expression and function of I region products on immunocompetent cells. II. I region products in T-B interaction.

The anti-Lac B precursor cells from BALB/c (H-2)d mice which survive cytotoxic treatment with anti-Iak and complement will respond to Lac-KLH in culture but require more KLH helper T cells than unselected B cell populations or B cells surviving anti-Ig killing. These findings are not explainable by the classical Poisson assumption of a constant target of T-B ionteraction. We propose a T-B interaction theory with variable Ia target on the B cell surface. The theory quantitatively predicts the observed dose response relationships, and implies that Ia molecules on B cells are cell interaction structures.

Animals↗

No direct association between Ia antigens and Fc receptors on the B cell membrane.

The capping of Ia antigens does not induce redistribution of Fc receptors (FcR) on B lymphocytes. This rules out the possibility of a unidirectional association between Ia and FcR such as has been reported to link Ig and FcR. Ia-capping was achieved with hapten-sandwich antibodies devoid of Fc regions: hapten-conjugated Fab anti-Ia followed by (Fab')2 anti-hapten antibody. Three different immune complex systems were used to label FcR. With fluorescent double labeling, Ia and FcR were readily distinguished. The independent labeling and surface mobility of Ia and FcR are considered in connection with reports of the inhibition of FcR by anti-Ia antibodies.

Animals↗

Expression and function of I region determinants on immunocompetent cells. I. Selective expression of I-C region determinants on immune cells.

We have examined the cytotoxic activity of anti-Iak serum and complement on various immune functions of BALB/c (H-2d) cells. Since the cytotoxic action of this antiserum on H-2d cells defines specificity Ia.7, an I-C region product, we have looked at the selective expression of this antigen. We have mainly used the in vitro anti-Lac2 response to study the cells involved in the induction and regulation of antibody. The data presented here show that Ia.7 is present on both IgM and IgG precursor B cells and in lesser amounts on plaque-forming cells. The antiserum also recognizes with less efficiency a product on specific T suppressor cells, which is possibly coded for by the adjacent I-J subregion. Both fluorescence and functional tests indicate the absence of Ia.7 on macrophages. It is also lacking on T helper cells. When we tested the antiserum on the in vitro cytotoxic responses to alloantigens, we found that neither T effector cells nor their precursors were affected.

Animals↗

[Injuries of the condylar cartilage of the knee in athletes].

The authors have observed 8 traumatic, isolated lesions of the articular cartilage of the medial condyle of the knee in young athletes (7 football players, one judoka). The clinical, radiological signs are described. Arthrographs were usually negative. On microscopical examination, the cartilage was not pathological. Excision of the fractured cartilage gave poor results.

Adult↗

Coexistence of helper and suppressor activities in carrier-primed spleen cells.

Both helper and suppressor activities for an in vitro IgG anti-hapten (Lac) response to Lac-HRBC were demonstrated in the same population of carrier (HRBC)-primed spleen cells. The relative radiosensitivity of suppressor activity permitted the selective removal of suppression and the demonstration of help. Both activities appear to be T cell-dependent and antigen-specific. Dilution analysis showed that help and suppression are mediated by distinct populations of cells.

Animals↗