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Biomedical subjects

C J Elson

Publications and source records attributed to C J Elson.

At least 145 records · Page 8Linked to original sources
PubMed1981

IgG antiglobulins in rheumatoid arthritis and other arthritides: relationship with clinical features and other parameters.

A radioimmunoassay has been developed for measuring IgG antiglobulins using baboon IgG as antigen. Raised levels were virtually confined to the sera of patients with rheumatoid arthritis (RA) and not found in other seronegative arthritides. High levels were found in both seropositive and seronegative (as judged by latex slide and sheep cell differential agglutination for IgM antiglobulins) patients with RA and were associated with systemic disease but not synovitis. Very high levels (more than twice the upper limit of normal) showed a strong association with vasculitis.

Antibodies, Anti-Idiotypic↗
PubMed1981

Tolerance to allotypic determinants induced by lymphoid cells from congenic mice bearing the allotype.

Mice of one allotype (Igb) were immunized against immunoglobulin from a congenic strain of mice bearing another allotype (Iga). This Igb anti-Iga response was profoundly suppressed by injecting lymphoid cells from congenic Iga mice but not by serum Iga. Suppression was specific, could be induced by congenic B cells but not histoincompatible lymphoid cells and depended both on the time of administration of cells relative to immunogenic challenge and to the number of cells injected. Unresponsiveness was more easily induced in neonates than adults. It is considered that tolerance to the allotype depends on the properties of the cells to which they are bound.

Animals↗
PubMed1981

IgG rheumatoid factor, complement and immune complexes in rheumatoid synovitis and vasculitis: comparative and serial studies during cytotoxic therapy.

IgG and IgM rheumatoid factors (IgG-RF and IgM-RF), complement and three assays for immune complexes were measured in 22 patients with rheumatoid arthritis (RA) complicated by either chronic active synovitis or vasculitis. Patients with vasculitis had relatively inactive arthritis but had higher titres of rheumatoid factors, especially IgG-RF, anticomplementary activity (ACA) and lower levels of C4 than those with synovitis. Clq-binding and platelet aggregation (PA) levels were similar in both groups. Serial measurements during cytotoxic therapy showed a close temporal relationship between the clinical features of vasculitis and levels of IgG-RF, ACA and C4 both with remission and with relapse. We suggest that immune complexes containing IgG-RF which activate complement and are detected by ACA are useful markers of rheumatoid vasculitis and may be important in its pathogenesis.

Antigen-Antibody Complex↗
PubMed1980

The isolation of immune complexes containing IgM rheumatoid factor and recovery of IgG rheumatoid factor from the complexes.

IgG with rheumatoid factor activity has been recovered from immune complexes containing IgM rheumatoid factor. This was done by passing serum from patients with rheumatoid arthritis through an immunoadsorbent column of the F(ab')2 fragment of rabbit anti-human mu chain. The recovered IgM was analysed by radioimmunoassays for IgM and IgG rheumatoid factors before and after sucrose density gradient centrifugation at neutral and acid pH. It is considered that the method may be generally applicable for the isolation of immune complexes containing IgM antibodies.

Animals↗
PubMed1980

Production of antibodies to host IgG after transfer of histocompatible cells primed to host allotype.

A method is described to bring about endogenous production of antibodies to the Fc region of IgG. Mice of one allotype (Igb) were immunized against immunoglobulin from a congenic strain of mice bearing another allotype (Iga). The Iga-primed cells were transferred to congenic recipients bearing the Iga allotype and the production of anti-host allotype antibodies by the donor cells measured. Low levels of anti-host allotype antibodies were found in the sera of normal recipients but much greater amounts in recipients pretreated with cyclophosphamide. On ultracentrifugation some of these IgG antibodies sedimented at more than 7S probably because they were complexed with the IgG antigen. It is considered that thismodel may be of use in testing the effect of anti-Fc antibodies on joint inflammation.

Animals↗
PubMed1980

Anti-erythrocyte autoantibody production in mice associated with the injection of rat erythrocytes.

Mice injected with rat erythrocytes developed anti-erythrocyte autoantibodies which reached a plateau at 4-12 weeks, then gradually declined until at about 24 weeks the majority of mice were negative. In such recovered mice re-challenge with rat erythrocytes produced an accelerated peak of autoantibody and a much more rapid return to a Coombs' negative state. The auto-antibody response was distinguished from the anti-rat response in being more radio-sensitive. Purified autoantibody reacted to higher titre with rat than with syngeneic erythrocytes. Lymphoid cells, from mice given rat erythrocytes (but not sheep, rabbit or guinea-pig erythrocytes) transferred to normal syngeneic recipients given rat erythrocytes suppressed autoantibody production in the recipients. This suppression was much more effective against the autoantibody response than against the response to the inducing cross-reactive antigen; and the degree of suppression was related to the number of cells transferred and to their time of administration relative to the injection of rat erythrocytes. The induction of autoantibody and the generation of suppressor cells in donor animals was unaffected by adult thymectomy. A comparison of the effect of anti-rat erythrocyte antibodies and spleen cells from rat-immunized donors on recipients responses to rat erythrocytes revealed that whereas anti-rat antibodies suppressed both the autoantibody and the anti-rat responses, the spleen cells suppressed only the autoantibody response. Populations of spleen cells, from rat immunized donors, depleted of B cells retained their suppressive activity, whereas the suppressive efficacy of T-cell depleted populations was reduced but not abolished. It is suggested that T cells can specifically interfere with thesponse of autoreactive B cells, although non-T cells (possibly B cells acting by an antibody-feedback mechanism) can also suppress their response.

Animals↗
PubMed1979

Low avidity as a cause of prozone phenomena.

The incidence of prozones was studied, under various conditions, in a model indirect haemagglutination system and in a radioimmunoassay--both assays depending on the use of anti-immunoglobulin (anti-Ig). It was found that prozones were correlated with the presence of low avidity antibodies, and that these could compete with high avidity antibodies for the limited amount of anti-Ig available. It is proposed that the relatively rapid dissociation of low avidity antibodies allows them to form immune aggregates with the anti-Ig. With increasing size these aggregates would become more susceptible to being washed off. In this way low avidity antibodies could occupy the anti-Ig, and yet be relatively ineffective, either for haemagglutination or for the binding of radioactively labelled (or fluorescein-labelled) anti-Ig to the antigen.

Animals↗
PubMed1979

Suppression of naturally occurring anti-tissue antibodies during growth and after removal of tumours.

The sera of normal rats were found to be active in the complement fixation test against isogeneic tumour homogenates. This activity was shown to be heat labile and to sediment with IgM globulins on zone ultracentrifugation in sucrose density gradients. Sera from rats bearing progressively growing tumours and sera from rats, which had such tumours excised, were found to be less active than normal rat sera in the complement fixation test against isogeneic tumour and liver homogenates. It was considered that this suppression of naturally occurring anti-tissue antibodies may be a specific process related to the host immune response to the tumour.

Animals↗
PubMed1978

Prevention of tolerance in differentiating B lymphocytes by T cells.

Normal, but not tolerant, adult thymocytes prevented particulate antigen inducing tolerance in differentiating B lymphocytes. This was demonstrated by measuring the emergence of responsive B cells (identified by their allotype) developing from a foetal liver innoculum in irradiated hosts with or without the addition of antigen, thymocytes or tolerant thymocytes. The relevance of these findings to the recruitment of B lymphocytes in adult animals and to the development of those autoreactive B cells found in normal animals is discussed.

Animals↗
PubMed1977

Tolerance in differentiating B lymphocytes.

These experiments demonstrate that the response of B lymphocytes to particulate antigen in vivo can depend on their stage of differentiation: B lymphocytes differentiating from stem cells were rendered tolerant, while mature B lymphocytes were primed under the same conditions. Lethally irradiated mice of one allotype were repopulated with 13-15 day fetal liver cells from congenic mice bearing another allotype and the effect of antigen on the emergence of responsive B cells determined. B cells, descended from the fetal liver inoculum (identified by their allotype) produced an antibody response to antigen in the presence of additional T cells, 15 days after transfer. Such a response could be prevented by injecting the recipient with alum-precipitated antigen (but not with deaggregated antigen) shortly after irradiation and reconstitution. This unresponsive state was specific and independent of afferent suppressor mechanisms. Mature B cells, on the other hand, were shown to be primed by alum precipitated antigen in irradiated reconstituted hosts. It was concluded that a fundamental difference exists between the responsiveness of mature and differentiating B lymphocytes. Tolerance in differentiating B lymphocytes is discussed in relation to the acquisition of self-tolerance.

Animals↗
PubMed1977

A suppressor mechanism controlling lymphocyte recruitment.

The duration of the inductive effect of an antigen (alum-precipitated trinitrophenyl-keyhole limpet haemocyanin) was measured, in the presence and absence of responding spleen cells, by transfering a test population of spleen cells to irradiated mice at various times relative to antigen injection. Using allotype-congenic mice, the response of a test (Iga) population was estimated in the presence of responding (Igb) cells. In the absence of responding cells the inductive effect fell to 10% of the peak value in 9-10 days, but in their presence it reached this level in less than 5 days. Removal of T cells from the responding (Igb) population reduced their suppressive efficacy. It was concluded that B lymphocyte recruitment is curtailed not by the elimination of antigen but by an active suppressor mechanism involving suppressor T cells.

Animals↗
PubMed1977

Cellular basis of persistent tolerance induced by an aggregate free heterologous immunoglobulin.

Attempts were made to break the tolerance of lymph node B cells to deaggregated human gamma globulin. Using allotype-congenic mice, lymph node cells from virgin or tolerant (5 mg) CBA/Igb donors were transferred tonormal CBA/Iga recipients and the proportion of responding donor B cells estimated 1 and 13 days later. The response of the non-tolerant virgin cells diminished with time but was still detectable at 13 days whereas the response of the tolerant cells was tenfold lower than normal cells at day 1 and was not detectable at 13 days. This functional deletion of tolerant cells was not reversed by enzymatic stripping of the immuno-globulin receptors before transfer, nor by removing T cells-which might have had a suppressor action. In other experiments Igb mice were thymectomized or left as controls at various times before tolerance induction. Lymph node cells from these mice were transferred, together with non-tolerant Iga cells, to irradiated recipients. The cell from tolerant thymectomized donors strongly suppressed the response of non-tolerant cells, whereas the tolerant control cells showed no suppressor activity. It is considered that B-cell tolerance can be maintained by something other than receptor blockade, or active suppression-although the latter can arise in some circumstances.

Animals↗
PubMed1976

Functional half-life of virgin and primed B lymphocytes.

The functional half-life, a measure of the persistence of lymphocytes in an antigen-free environment, has been estimated and found to be about 7 days for virgin 2,4,6-trinitrophenyl (TNP)-reactive mouse B cells, and 2--3 times longer for TNP-primed B cells. Using allotype-congenic mice, lymph node cells were transferred from virgin or primed CBA/Igb donors to normal CBA/Iga recipients, and the proportion of donor B cells estimated at intervals...

Animals↗
PubMed1975

Permanent hapten-specific tolerance in B lymphocytes.

Tolerance to the hapten TNP was induced in mice congenic with CBA but bearing the Ig-b allotype (Ig-b mice). To induce a high degree of tolerance it was necessary to give five injections of TNP-sulphonate followed by an immunogenic challenge (alum precipitate of TNP-BSA with pertussis adjuvant). Lymph node or spleen cells from these mice were transferred, with or without an equal number of non-tolerant CBA spleen cells, to irradiated CBA recipients and these were challenged with a different TNP-protein conjugate. Anti-TNP antibody bearing the Ig-b allotype was then assayed separately from total anti-TNP, as a measure of the contributions made by tolerant and non-tolerant B-cell populations respectively. Tolerant lymph node cell did not depress the response of normal cells, nor did the normal cells 'break' the tolerance of the Ig-b population even when the latter had been treated with anti-T-cell serum and complement. No response was obtained from tolerant lymph node cells when the recipients were challenged at different time up to 12 weeks after transfer. By this time the control non-tolerant lymph node cells had also lost the capacity to respond. It is concluded that: (1) effectively permanent tolerance, which is not maintained by afferent mechanisms, can be induced in lymph node B cells; (2) B-cell tolerance can be greatly enhanced by immunogenic challenge; (3) spleen may contain a distinct population of B cells which is less susceptible to tolerance; and (4) the life-span of virgin lymph node B cells is probably less than 12 weeks.

Animals↗