immunoglobulins of any isotype with antibody activity directed against antigenic sites on the Fc region of human or animal IgG associated with three major immunoglobulin classes, IgM, IgG, and IgA Immunoglobulin M rheumatoid factor is manifested in approximately 70% of adults but is not specific for RA. Being RF-positive correlates with the following: Severity of the disease (in general) Nodules Other organ system involvement (e.g., vasculitis, Felty’s syndrome, Sjögren’s syndrome) Agglutination tests for RF, such as the sensitized sheep cell test and latex agglutination, generally detect IgM RFs. Latex agglutination is sensitive but can produce a fairly high number of false-positive results. Because conventional procedures are semiquantitative, they may be insensitive to changes in titer and may detect only those RFs that agglutinate. associated: hepatitis parasitic disease infectious mononucleosis subacute bacterial endocarditis tuberculosis cancer Elevated values may also be observed in the normal older population. The concentration of RF tends to be highest when the disease peaks and tends to decrease during prolonged remission. RESEARCHER: REFERENCE/S: Turgeon, M. L. (2014). Immunology & Serology in Laboratory Medicine (5th ed.). Missouri: Elsevier Inc. page 429.
2) Describe the pathophysiology of Rheumatoid Arthritis
a chronic, multisystemic, autoimmune disorder and a progressive inflammatory disorder of the joints a highly variable disease that ranges from a mild illness of brief duration to a progressive destructive polyarthritis associated with a systemic vasculitis Prevalence increases significantly with age Persons with the human leukocyte antigen (HLA)–DR4 haplotype have a significantly higher incidence of RA. Females > males Non- Hispanic whites, blacks, Native Americans, and Alaska Natives > Hispanics, Asians, and Pacific Islanders. Obese and overweight people > underweight or normal weight individuals. Physically inactive people > physically active people. Progression: a. Initiation of synovitis by the primary causative factor b. Subsequent immunologic events that perpetuate the initial inflammatory reaction. c. Transition of an inflammatory reaction in the synovium to a proliferative, destructive tissue process Pathogenesis an infective agent or other stimulus binds to receptors on dendritic cells (DCs), which activates the innate immune system DCs migrate into lymph nodes and present antigen to T lymphocytes, which are activated by two signals— the presentation of antigen and costimulation through CD28. Activated T lymphocytes proliferate and migrate into the joint. Subsequently, T lymphocytes produce interferon-γ (IFN-γ) and other proinflammatory cytokines. This in turn stimulates macrophages and other cells, including B lymphocytes. B cells appear to be pivotal in the pathogenesis of RA because they can be 10,000 times as potent as DCs in presenting antigen. Stimulated macrophages and fibroblasts release cytokines, including tumor necrosis factor-α (TNF-α), a central component in the cascade of cytokines. This results in the production of additional inflammatory mediators and further recruitment of immune and inflammatory cells into a joint. Anti–TNF-α treatment strategies (e.g., monoclonal) prevent interaction with receptors on cell surfaces. The leukotrienes play a major role in the inflammatory response to injury. This class of biologically active molecules has been implicated in the pathogenesis of RA and in other inflammatory diseases.
RESEARCHER: COLTING, Frilyn Joyce S.
REFERENCE/S: Turgeon, M. L. (2014). Immunology & Serology in Laboratory Medicine (5th ed.). Missouri: Elsevier Inc. pages 425-428.
3) Describe the nature of autoimmune disease
Autoimmunity represents a breakdown of the immune system’s ability to discriminate between self and nonself. The term autoimmune disorder refers to a varied group of more than 80 serious, chronic illnesses that involve almost every human organ system. In all these disorders, the underlying problem is similar; the body’s immune system becomes misdirected, attacking the organs it was designed to protect. The term autoimmune disorder is used when demonstrable immunoglobulins (autoantibodies) or cytotoxic T cells display specificity for self antigens, or autoantigens, and contribute to the pathogenesis of the disorder. Autoimmune disorders are characterized by the persistent activation of immunologic effector mechanisms that alter the function and integrity of individual cells and organs. The sites of organ or tissue damage depend on the location of the immune reaction. The variety of signs and symptoms seen in patients with autoimmune disorders reflects the various forms of the immune response.
RESEARCHER: REFERENCE/S: Turgeon, M. L. (2014). Immunology & Serology in Laboratory Medicine (5th ed.). Missouri: Elsevier Inc. page 383.