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Biomedical subjects

R S Krakauer

Publications and source records attributed to R S Krakauer.

At least 19 recordsLinked to original sources
PubMed1985

The influence of thymic humoral factor on systemic lupus erythematosus lymphocyte function.

The influence of thymic humoral factor, THF, on systemic lupus erythematosus, SLE, lymphocyte function was investigated. Increasing numbers of SLE T-cells, rosetted at 4 degrees C or 37 degrees C, were cultured with allogeneic normal B-cells and the change in IgM synthesis was assessed. Lymphocytes of some SLE patients showed improved suppression with THF when rosetted at 37 degrees C. Normal control lymphocytes did not show a net change in suppression with THF. The subgroup of SLE patients that showed improved suppression with THF in vitro might be a more appropriate group for in vivo therapeutic trials with thymic hormone, TH, than SLE patients in general.

B-Lymphocytes↗
PubMed1983

Therapeutic trial of cryofiltration in patients with rheumatoid arthritis.

Cryofiltration, a new technique for on-line plasma separation and its treatment by cold filtration, enables the selective removal of immune complexes and eliminates the need for replacement proteins. Fifteen patients with rheumatoid arthritis were treated for nine to 10 consecutive sessions over a three- to five-week period. Circulating immune complexes decreased by an average of 78 percent and rheumatoid factor by 32 percent. This was accompanied by significant clinical improvement in morning stiffness, articular index, 50-foot walking time, grip strength, and target joint circumference. Cryofiltration might thus be beneficial for a subgroup of rheumatoid arthritis patients in whom conventional therapy has failed.

Arthritis, Rheumatoid↗
PubMed1981

Abnormalities of immunoregulation in progressive systemic sclerosis. Evidence for excess helper-cell function and altered B-cell function.

We investigated immunoregulatory function in patients with progressive systemic sclerosis (PSS) in terms of in vitro IgM synthesis. Suppressor-cell function seems normal in regard to the ability of concanavalin A-treated cells to inhibit IgM synthesis by normal cells. At 4 x 10(5) T cells to 3 x 10(5) allogeneic normal B cells per milliliter, T cells from patients with PSS induce significantly more IgM synthesis by normal B cells than do normal T cells. This increased helper T-cell function might be involved in the pathogenesis of the disease.

Adult↗
PubMed1980

Suppressor cell function in psoriasis.

Recent studies suggest that autoimmunity may play a role in the pathogenesis of psoriasis. In view of these findings, it is postulated that the immunologic defect may be associated with regulation of the immune system. A study was undertaken to determine whether a suppressor cell defect was present. Two groups of patients with active psoriasis who were receiving no therapy were selected. Peripheral blood lymphocytes were pulsed with concanavalin A, 40 microgram/cc, for 48 hours. Their ability to suppress a mixed lymphocyte reaction with both autologous and allogeneic responding cells was assessed. There was a significant decrease in suppressor activity in psoriasis patients compared with normal individuals. Although we have not demonstrated that this mechanism is implicated directly in a causal relationship to psoriasis, it nevertheless gives further support to the possible role of the immune system in the pathogenesis of psoriasis.

Concanavalin A↗
PubMed1980

Suppressor cell defect in SLE: relationship to native DNA binding.

Recent evidence suggests the presence of a suppressor T cell defect in systemic lupus erythematosus. We confirm the presence of such a defect and find a strong quantitative correlation between the loss of suppressor T cell function and the activity of SLE as measured by the presence of antibodies to native DNA. In addition, the serum of patients with active SLE contains a soluble factor which when incubated with normal peripheral blood lymphocytes induces a suppressor T cell defect. These data are consistent with the suppressor cell defect being involved in the propagation and possible the pathogenesis of SLE, and suggests a positive feedback mechanism whereby a suppressor cell defect results in autoantibodies including antibody to suppressor cells.

Adult↗
PubMed1980

Suppression of polyclonal immunoglobulin biosynthesis by a soluble factor: T-cell dependent and T-cell independent mitogens.

When normal human spleen cells are pulsed with concanavalin A (Con A), a portion become suppressor cells which in co-culture can inhibit immunoglobulin synthesis by other normal spleen cells stimulated by pokeweed mitogen (PWM). One mechanism whereby these Con-A activated spleen cells suppress Ig synthesis appears to be by the secretion of a soluble suppressor factor(s) since supernatants of Con-A stimulated splenocytes also suppress the polyclonal synthesis of immunoglobulin by human spleen cells. In this study, we report that supernatants of Con-A activated spleen cells suppress the in vitro synthesis of IgG, IgM and IgA by human spleen cells cultured with PWM. Our results indicate that the soluble suppressor factor(s) blocks an early stage in the differentiation of B lymphocytes into plasma cells without affecting the synthesis and secretion of immunoglobulin by more mature lymphocytes which appear to be irreversibly committed toward the pathway of synthesizing immunoglobulin. In addition, we studied the ability of normal human spleen cells to synthesize polyclonal immunoglobulin when cultured with either the T-cell dependent PWM or T-cell independent mitogens lipopolysaccharide (LPS) and Nocardia. Our results demonstrate that normal human splenic mononuclear cells cultured with either Nocardia, LPS or PWM are significantly stimulated to synthesize polyclonal IgG, IgM and IgA. Furthermore, supernatants of Con-A activated human spleen cells suppressed the polyclonal synthesis of these three antibody classes by human spleen cells responding to either T-cell dependent or independent mitogens.

Cell Survival↗
PubMed1979

A quantitative assay for low levels of IgM by solid-phase immunofluorescence.

A quantitative immunofluorescent assay capable of detecting between 15 and 1450 ng of IgM on a strictly linear standard curve has been developed. The assay system is unique in that in vitro biosynthesized polyclonal IgM in culture supernatants can be quantitated with a minimal quantity of supernatant. Interference created by lectins and bead-surface interactions have been analyzed. This easily operated assay has been validated and is reliable. A very important feature of the system is the considerable cost reduction in comparsion with radiometric techniques.

Antibodies, Anti-Idiotypic↗
PubMed1978

Loss of suppressor T cells in the pathogenesis of the autoimmunity of NZB/W mice.

Loss of suppressor T cells was demonstrated in NZB/W mice, an animal model of autoimmunity. As NZB/W mice matured they lost splenic T cells that could be activated by concanavalin A (Con A) to become suppressor cells and lost the ability to produce the regulator of humoral immune responses, soluble immune response suppressor (SIRS). However, NZB/W spleen cells retained the capacity to respond to suppressor signals from Con A pulsed normal spleen cells. Thrice weekly administration of SIRS containing supernatants of Con A pulsed normal spleen cells to young NZB/W mice lead to a striking reduction in the manifestations of autoimmunity.

Aging↗
PubMed1978

Disorders of suppressor immunoregulatory cells in the pathogenesis of immunodeficiency and autoimmunity.

A series of suppressor cell systems regulate virtually all immunologic processes. Disorders of these systems have been identified in association with a number of diseases. An abnormal number of activated suppressor T-cells have been seen in some patients with common variable hypogammaglobulinemia and in some with selective IgA deficiency. Suppressor T-cells that inhibit immunoglobulin synthesis also develop in an animal model of immunodeficiency, the agammaglobulinemia of the bursectomized bird. Non-T-cell suppressor cells are a pathogenic factor in the humoral immunodeficiency associated with multiple myeloma. At the other end of the spectrum of immunologic response, a reduction in functional activity of suppressor T-cells has been implicated in the pathogenesis of autoimmune diseases. The disorders of suppressor cells that have been shown in immunodeficiency and autoimmunity are important when developing rational strategies for prevention and therapy of these immunologic disorders.

Agammaglobulinemia↗