Cells In Rheumatoid Arthritis Patients Research Articles

Lymphocytes bearing Fc gamma receptors in rheumatoid arthritis. I. An increased subpopulation of cells in rheumatoid arthritis detected with Facb rosettes.

The chronic production of IgM and IgG antiglobulins is a major feature of rheumatoid arthritis. This implies an abnormal interaction between rheumatoid leucocytes and IgG. A novel rosette assay employing rabbit Facb-coated calf red blood cells has been developed to study receptors for IgG on peripheral blood lymphocytes. Cells were obtained from groups of patients with rheumatoid arthritis (RA), osteoarthritis (OA), ankylosing spondylitis (AS), and healthy control subjects. Receptors for Facb were found on an increased proportion of lymphocytes from RA patients compared with the other groups tested. It has been shown that the Facb rosette assay detects a subpopulation of lymphocytes bearing receptors for the Fc region of IgG. This receptor is clearly capable of recognising and binding only the C gamma 2 domain within the Fc region. As such it shows different specificity from some other Fc receptors detected on mononuclear cells. The number of Facb rosette-forming lymphocytes in an individual sample correlated well with the number of cells bearing 'high avidity' Fc receptors. However, the incidence of these cells in RA patients could not be correlated with disease activity, disease duration, or levels of IgM and IgG rheumatoid factor. Thus increased Facb rosette cells may represent a fundamental imbalance of the immune response in patients with rheumatoid arthritis.

Demonstration of anti-rubella antibody-secreting cells in rheumatoid arthritis patients.

In the present study we describe a plaque-forming cell assay using erythrocytes coated with viral antigen, which detected anti-viral antibody-secreting cells against various viral antigens. These anti-viral antibody-secreting cell were studied in normal individuals with known viral infections and in rheumatoid arthritis patients. Rubella anti-viral antibody-secreting cells were present after induction in the peripheral blood of eight out of ten patients. No plaques were seen before induction. Synovial tissue of seven patients out of ten showed rubella-antigen-specific plaques before induction. In all three patients tested, the numbers of plaques increased after induction. The peripheral blood of only one patient showed plaque-forming cells against mumps virus and cytomegalovirus (CMV) antigen. No other patients showed any plaque against CMV, respiratory syncytial virus, mumps virus, measles virus, adenovirus, and varicella zoster virus antigens. The method appears to be promising in studying viral antibody-secreting cells in human immunopathology.

A study of coronary flow under conditions of hemorrhagic hypotension and shock: Opdyke, David F., and Foreman, Robert C.: am. J. Physiol. 148:726 (March), 1947

Human CD4+ T cells can be classified as either naïve, central memory (TCM), or effector memory (TEM) cells. To identify the CD4+ T cell subsets most important in the pathogenesis of rheumatoid arthritis (RA), we phenotypically defined human CD4+ T cells as functionally distinct subsets, and analyzed the distribution and characteristics of each subset in the peripheral blood. We classified CD4+ T cells into six novel subsets based on the expression of CD45RA, CCR7, CD27, and CD28. The CCR7 + CD45RA–CD27 + CD28+ TCM subset comprised a significantly smaller proportion of CD4+ T cells in RA patients compared to healthy controls. The frequency of TNF-α-producing cells in the CCR7–CD45RA–CD27 + CD28+ TEM subset was significantly increased in RA. Furthermore, within the CCR7 + CD45RA–CD27 + CD28+ TCM subset, which was decreased in periperal blood from RA, the proportions of total Foxp3+ Treg cells and CD45RA–Foxp3high activated/effector Treg cells were significantly lower in RA patients. Our findings suggest that the increased proportion of TNF-α-producing cells and the decreased proportion of CD45RA–Foxp3high activated/effector Treg cells in particular subsets may have critical roles in the pathogenesis of RA.