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Biomedical subjects

R A Good

Publications and source records attributed to R A Good.

At least 721 records · Page 40Linked to original sources
PubMed1976

Lupus erythematosus-like syndrome with a familial deficiency of C2.

Several cases of isolated C2 deficiency in man have been reported in the medical literature. The earliest cases did not seem to be associated with known diseases or syndromes; more recently, reports of C2 deficiency associated with systemic lupus erythematosus; anaphylactoid purpura, recurrent infections, and dermatomyositis have appeared. We report here another case of C2 deficiency. The propositus, a 24-year-old woman, had a lupus erythematosus-like rash and a history of arthralgia, as well as a selective deficiency of C2. Studies of hemolytic C2 of the immediate members of her family indicate an autosomal-recessive mode of inheritance. These findings add to the increasing evidence that a C2 deficiency predisposes some persons to serious vascular diseases.

Adult↗
PubMed1976

Leukocyte migration inhibitory factor (LMIF) production in unidirectional mixed lymphocyte cultures.

Puromycin treatment of lymphocytes was used to develop a one-way test for leukocyte migration inhibitory factor (LMIF) production in the mixed lymphocyte culture (MLC) reaction. Lymphocytes incubated with this protein synthesis inhibitor induced a vigorous mediator production by nontreated allogeneic cells, being themselves unable to respond to stimulator cells. When puromycin-treated cells were stimulated with the mitogens PHA, ConA, or PWM, overall protein and DNA synthesis were significantly decreased with concomitant abolishment of LMIF production. Viability of stimulator lymphocytes was found to be essential for generation of the mediator in MLC reaction.

Cell Survival↗
PubMed1976

Influence of protein restriction on immune functions in NZB mice.

The influence of a low protein (6%) diet on the immunologic function of NZB mice was investigated. The low protein intake was associated with decreased weight gain in both male and female NZB mice. The mice fed the low protein diet did not develop splenomegaly, which generally occurs by 7 to 10 months of age in NZB mice fed a normal amount of protein. Further, 7- to 10-month-old NZB mice fed the low protein(6%) diet, maintained: 1) more vigorous antibody production to sheep red blood cells; 2) greater capacity to produce graft-vs-host reactions, and 3) more vigorous cell-mediated "killer" cell immunity after immunization against DBA/2 mastocytoma cells than did NZB mice on a normal (22%) protein diet. The decrease of PHA and Con A response which normally occurs with aging in NZB mice was abrogated to some degree by protein restriction. However, response to LPS, which also declines with age in NZB mice, did not appear to be influenced by diet.

Animals↗
PubMed1976

Heterogeneity of stem cells in severe combined immunodeficiency.

Two patients with severe combined immunodeficiency disease (SCID) having variable B-cell development have been shown to have marrow precursors of lymphoid cells which can be induced in vitro by thymic factors to express certain T-cell surface characteristics (HTLA+ phenotypes). Their marrow cells could not, however, be induced by these same factors to develop the E-rosette marker or functional activities of T lymphocytes. The marrow of these children also showed, when compared to that of normal adults, a different distribution of cellular elements on density gradient fractionation. The findings support the view that the disorder under study has a different pathogenesis from other forms of SCID previously analysed.

Age Factors↗
PubMed1976

Leukocyte migration inhibitory factor (LMIF) profile in primary and secondary immunodeficiency disease.

Lymphocytes from patients with primary and secondary immunodeficiency disease were tested for capacity to produce LMIF after mitogen and antigen stimulation as well as for ability to stimulate and respond in unidirectional MLC-LMIF assay. Different patterns of immune abnormality in vitro were detectable when Con A and Candida albicans antigen were used. In addition, significant abnormalities in LMIF responding and stimulatory capacity were demonstrated in patients with Hodgkin's disease. LMIF production after stimulation with different agents allows for a better characterization of cellular defects in immunodeficiency disease.

Antigens, Fungal↗
PubMed1976

Immunology.

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Allergy and Immunology↗
PubMed1976

Nutritional deficiency, immunologic function, and disease.

Several experiments conducted by our group over a period of 6 years have shown that nutritional stress, especially protein and/or calorie deprivation, leads to many, often dramatic, changes in the immune responses of mice, rats, and guinea pigs. Chronic protein deprivation (CPD) has been shown to create an enhancing effect on the cell-mediated immune responses of these animals. Humoral responses under CPD conditions were most often found to be depressed, but sometimes were unaffected, depending on the nature of the antigen employed. Chronic protein deprivation, consistent with the pattern just mentioned, improved tumor immunity by depressing production of B-cell blocking factors, and, in at least one instance, resistance to development of mammary adenocarcinoma in C3H mice was associated with evidence of increased numbers of T suppressor cells. Profound nutritional deficits (less than 5% protein per total daily food intake) depressed both cellular and humoral immunity. Early, though temporary, protein deprivation caused a long-term depression of both cellular and humoral immunity also, with the humoral component being the first to recover. Manipulation of protein and calories was found to have a profound effect on certain autoimmune conditions. Diets high in fat and low in protein favored reproduction but shortened the life of NZB mice, whereas diets high in protein and low in fat inhibited development of autoimmunity and prolonged life. Chronic moderate protein restriction permitted NZB mice to maintain their normally waning immunologic functions much longer than mice fed a normal protein intake. Further, the low-protein diet was associated with a delay in development of manifestations of autoimmunity. Decreasing dietary calories by a reduction of fats, carbohydrates, and proteins more than doubled the average life span of (NZB X NZW)F1 mice, a strain prone to early death from autoimmune disease. Histopathologic studies using immunofluorescent microscopy revealed that the development of the renal lesions caused by the deposition of antigen-antibody complexes, which is so characteristic of these mice, was markedly delayed.

Anemia, Hemolytic↗
PubMed1976

Surface markers of human eosinophils.

Peripheral blood eosinophils from patients with eosinophilia and from healthy subjects were studied for surface immunoglobulins, receptors for the Fc region of IgG, complement receptors, and spontaneous rosette formation with sheep and mouse erythrocytes. Eosinophils were found to have receptors for complement and for aggregated IgG, and to have the same two types of complement receptors as do lymphocytes and monocytes. Immune adherence type receptors were specific for C4 or C3b, while C3d receptors were specific for C3d but unreactive with C4. Eosinophils differed from fully mature neutrophils in that the former had C3d receptors and relatively weak immune adherence (C4 or C3b) receptors, while the later did not have the C3d receptors and had strong immune adherence receptors. Eosinophil phagocytosis of complement-receptor bound erythrocytes was dependent on the presence of IgG in the antibody coating the red blood cells; this requirement for IgG resembled that found in neutrophil phagocytosis. No surface Ig or spontaneous erythrocyte rosette formation was observed with eosinophils.

Binding Sites, Antibody↗
PubMed1976

Leukocyte-derived complement inhibitor. IV. The functional properties of C1 bound to erythrocytes pretreated with leukocyte culture supernatant.

E, pretreated with leukocyte cultures supernatant (ES), binds C1 through C1q; ES and EIgM that bind the same amount of C1 as measured in a hemolytic assay have the same uptake of 125I-C1q; ESC1q and EIgMC1q, carrying the same number of molecules of CUq per cell, have the same uptake of CUr and CUs; soluble immune compleses prevent the binding of C1 and C1q to ES. The activity of C1 bound to ES is impaired; ESC1 can react with C4 but not with C2. The C4 turnover and the C1 ING turnover by ESC1 are reduced so that ES-bound C1 is protected from destruction by C1 ING. These modifications are fully reversed when C1 is transferred from ES to EA:C1 recovers its ability to react with C2, and C1 INH. Thus the C1s activity can be modulated inside the C1 molecular complex upon binding of C1q to a lymphocyte product. In addition, the 125I-C1q uptake is proportional to the amount of IgM hemolysin used to sensitize E; it has, however, an exponential relationship to the amount of IgG or S used to sensitize E. The ratio of 125I-C1q uptake towhole C1 uptake measured in a hemolytic assay is lowerthan 2. This indicates that one molecule of IgM is sufficient to bind one molecule of C1q on E, that several molecules of IgG or S are required to bind one molecule of C1q, and that one molecule of C1q is sufficient to create a lytic site on E.

Animals↗
PubMed1976

Circadian rhythmic plaque-forming cell response of spleens from mice immunized with SRBC.

Studies under controlled conditions of lighting and temperature revealed clear evidence of circadian periodicity with respect to the number of PFC present in the spleens of BALB/c mice 3 or 4 days after immunization with SRBC. Striking differences in proliferative responses of spleen lymphocytes to PHA or Con A were also observed at two different circadian times. Large proliferative responses occurred at the time when injection of antigen and/or sampling for PFC yielded a low PFC formation (early in the daily dark span) and small proliferative responses occurred at the time when antigen injection and sampling yielded high formation of PFC (early in the daily light span). These findings indicate that care should be taken to control the circadian timing of stimulation and sampling in studies of immune responses, and that rhythmically varying aspects constitute a new dimension of immunologic processes awaiting further analysis in both the circadian and weekly spectral regions.

Animals↗
PubMed1975

Mixed lymphocyte culture determinants and C2 deficiency: LD-7a associated with C2 deficiency in four families.

Four families with C2 deficiency were studied. Among eight HL-A haplotypes involved with C2 deficiency, five were HL-A 10,W18. Three homozygotes for C2 deficiency from different families were mutually nonreactive in mixed lymphocyte cultures (MLC) and the heterozygotes from the fourth family failed to react to the homozygous cells. It appeared that identical MLC determinants were associated with all the genes from the different families that related to C2 deficiency. Further experiments identified the MLC determinant, LD-7a, as being involved. These results suggest marked linkage disequilibrium between the genes for C2 deficiency and the major histocompatibility complex (MHC). Studies of possible recombinants have offered tentative evidence for the positioning of the locus for C2 deficiency with respect to other segments of the MHC.

Chromosome Mapping↗