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Biomedical subjects

A Gibofsky

Publications and source records attributed to A Gibofsky.

At least 37 records · Page 2Linked to original sources
PubMed1991

Assessing the impact of self-efficacy beliefs on adaptation to rheumatoid arthritis.

This article examines the influence of self-efficacy beliefs on problem-solving coping, functional disability, and psychological well-being for 101 recently diagnosed adult patients with rheumatoid arthritis (RA). Data were drawn from a longitudinal study of psychosocial adaptation to the onset of RA. Self-efficacy beliefs were associated with less functional disability assessed concurrently and 1 year later. Self-efficacy beliefs were also associated with greater use of problem-solving coping 1 year later. There was an interaction between pain and self-efficacy beliefs in the prediction of depression 1 year later: at low pain, self-efficacy beliefs were unrelated to depression, but at higher levels of pain, greater self-efficacy was related to greater depression. Finally, problem-solving coping mediated the relationship between disability and initial self-efficacy beliefs. The distinct patterns that emerge for pain, self-efficacy beliefs, and coping, with respect to functional status as compared to psychological status, are discussed.

Adaptation, Psychological↗
PubMed1991

Social support as a double-edged sword: the relation of positive and problematic support to depression among rheumatoid arthritis patients.

This study considers social network interactions as a potential source of both stress and support for individuals coping with a chronic illness. The sample consisted of 101 recently-diagnosed rheumatoid arthritis patients. Symptoms of depression were assessed using the Center for Epidemiologic Studies Depression scale. Hierarchical multiple regression analyses examined the conjoint effects of social support and problematic interactions on symptoms of depression. Receipt of positive or helpful support from close friends and family was related to lower depression; receipt of problematic support was related to increased depression. A positive x problematic support interaction suggested that the costs of problematic support do not cancel out the benefits of positive support. Patients who reported both little support and a greater degree of problematic interactions experienced the highest level of symptoms. The findings emphasize the need to consider positive and negative aspects of support transactions conjointly in assessing their stress-reducing and health-protective potential.

Adaptation, Psychological↗
PubMed1991

The genetics of rheumatic fever: relationship to streptococcal infection and autoimmune disease.

A large body of evidence suggests that patients with rheumatic fever immunologically respond abnormally both at a humoral and cellular level to streptococcal antigens cross-reactive with mammalian tissues. Implicit in this concept is that this abnormal immune response is genetically programmed. Using a monoclonal antibody called D8/17, a B cell marker has now been identified in 90-100% of all patients with rheumatic fever tested in 5 different geographical and ethnic populations. This trait appears to be inherited in an autosomal recessive fashion. This recognition of a B cell marker unique to individuals with rheumatic fever has important public health implications with respect to identification of individuals susceptible to rheumatic fever, possible prevention of disease and the recognition of prime candidates for future streptococcal vaccines.

Autoimmune Diseases↗
PubMed1989

Rheumatic fever.

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Humans↗
PubMed1989

Presence of a non-HLA B cell antigen in rheumatic fever patients and their families as defined by a monoclonal antibody.

Numerous investigators have suspected that there is a genetic predisposition to rheumatic fever (RF). In this context we have recently produced a series of monoclonal antibodies directed against B cells obtained from RF patients one of which, labeled D8/17, identifies a B cell antigen present in 100% of all RF patients studied. While the highest percentage of positive cells were exhibited by RF probands (33.5% +/- SE), the percentage of cells in unaffected siblings and parents was 14.6 and 13%, respectively. The percentage of positive cells in APSGN probands, unaffected siblings, and parents was 2.96, 3.86, and 2.8%, respectively. A low level of B cells (5-7%) bearing the D8/17 marker was seen in control patients. The segregation pattern of the phenotypes defined by the percentage of D8/17 positive cells within HLA-typed RF families are consistent with an autosomal recessive mode of inheritance not associated with the human MHC system. We postulate that these phenotypes indicate the presence of at least one necessary genetic factor for susceptibility to RF.

Analysis of Variance↗
PubMed1986

Altered phagocytosis by monocytes from HLA-DR2 and DR3-positive healthy adults is Fc gamma receptor specific.

Fc gamma receptor-dependent mononuclear phagocyte system (MPS) clearance of opsonized erythrocytes is prolonged in healthy adults with the class II alloantigens HLA-DR2, DR3, or DQw1, despite normal receptor-specific Fc ligand binding by monocytes in these groups. To investigate the basis for the MPS dysfunction, we determined the phagocytic capacity of blood monocytes from 66 disease-free adults and analyzed the data according to the HLA type of the subjects. The data demonstrate decreased phagocytosis of IgG-sensitized erythrocytes (EA) by monocytes from HLA-DR2, DR3, or DQw1-positive subjects compared with normals without these B cell alloantigens (2.87 +/- 0.83 erythrocytes/monocyte vs 3.87 +/- 1.05, p less than 0.004; 3.01 +/- 0.94 vs 3.87 +/- 1.05, p less than 0.02; 3.18 +/- 0.89 vs 3.87 +/- 1.05, p less than 0.02, respectively). Because HLA-DR2 and DQw1 are in linkage disequilibrium, we compared EA phagocytosis in subjects with DQw1 alone to normals without HLA-DR2, DR3, or DQw1. Among subjects positive only for DQw1, no significant decrease in phagocytosis could be seen (3.46 +/- 0.95 vs 3.87 +/- 1.05, p = NS). To determine whether these differences represented an Fc receptor-specific dysfunction or a more generalized decrease in phagocytic activity, we compared the quantitative phagocytosis of EA with that of neuraminidase-treated erythrocytes (EN), which is Fc receptor independent and beta-glucan receptor mediated. No segregation of phagocytic capacity for EN by HLA class II phenotypes could be demonstrated (DR2, 2.68 +/- 1.30 erythrocytes/monocyte; DR3, 2.95 +/- 1.30; DQw1, 2.84 +/- 1.15; others, 3.06 +/- 1.14). Our data indicate that the decrease in phagocytosis by blood monocytes from normal individuals with HLA-DR2 or DR3, the class II alloantigens associated with systemic lupus erythematosus and other autoimmune diseases, is specific for the Fc receptor-mediated process. This alteration of Fc receptor function among immunogenetically defined individuals may contribute to their predisposition to autoimmune disease. These differences may also apply to other Fc receptor-initiated cellular functions.

Adult↗
PubMed1984

Defective mononuclear phagocyte function in systemic lupus erythematosus: dissociation of Fc receptor-ligand binding and internalization.

Fc receptor-mediated mononuclear phagocyte system (MPS) clearance is impaired in systemic lupus erythematosus (SLE) and may contribute to the pathogenesis of the immune complex disease. To investigate the basis of MPS dysfunction, we have examined concurrent in vivo and in vitro Fc receptor function in 22 patients with SLE and 23 disease-free adults. Blood monocyte Fc receptor binding was increased rather than decreased as predicted by the saturation hypothesis of MPS blockade. Rosette formation of IgG-sensitized bovine erythrocytes (EA) with monocytes demonstrated increased Fc receptor-ligand binding in SLE (percent rosettes: 40 +/- 12 vs 27 +/- 8, p less than 0.001). Scatchard analysis of the binding of radiolabeled IgG oligomers to SLE monocytes indicated a mean receptor number 30% higher than control, although this did not reach statistical significance. Despite enhanced Fc receptor-ligand (EA) binding, Fc-mediated phagocytosis of EA was decreased in SLE (1.7 +/- 0.7 erythrocytes/monocytes/hour vs 2.6 +/- 1.0, p less than 0.004). This decrease in phagocytosis by blood monocytes from SLE patients was significantly greater than that attributable to the predominance in SLE of individuals with certain HLA B cell alloantigens and intrinsically lower phagocytic rates (p less than 0.05 for all groups). This decrease therefore represents a disease-acquired characteristic. Furthermore, the phagocytic rate of the four SLE patients with marked prolongation in MPS clearance was significantly lower than that of the eight patients with near normal clearance values (p less than 0.01). Saturation of Fc receptors by immune complexes does not explain impaired immune clearance in SLE. Our results indicate that despite increased binding of the EA ligand, Fc receptor-mediated phagocytosis is markedly impaired in SLE monocytes. This impairment cannot be explained on the basis of HLA-related differences in phagocytosis among lupus patients. The defect in phagocytosis of EA is most profound in those patients with the most significantly impaired MPS clearance. Thus, the dissociation of receptor-ligand binding and receptor-mediated internalization may contribute significantly to the in vivo clearance defect in SLE.

Adult↗
PubMed1983

Impaired fc-mediated mononuclear phagocyte system clearance in HLA-DR2 and MT1-positive healthy young adults.

Normal individuals with an HLA haplotype containing either DR2, MT1, or B8/DR3 are more likely to have abnormally prolonged Fc receptor-mediated mononuclear phagocyte system (MPS) clearance of IgG-sensitized autologous erythrocytes than their normal counterparts without such haplotypes. Although measurement of Fc receptor binding by rosette formation and saturable IgG aggregate binding revealed no differences among groups, Fc receptor-mediated phagocytosis of IgG-sensitized bovine erythrocytes by monocytes was decreased in the DR2-positive and MT1-positive individuals. The basal in vivo MPS clearance in normal individuals may be immunogenetically determined and may reflect differences in phagocytic rates.

Adult↗